{"title":"Oncology Signaling — Vectors \u0026 Viruses","description":null,"products":[{"product_id":"p53-reporter-lentivirus-bhv19400007","title":"P53 Reporter Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eTP53 encodes p53, a tumor suppressor transcription factor often described as the guardian of the genome. In response to cellular stresses such as DNA damage, oncogene activation, and hypoxia, p53 is stabilized and binds specific response elements to activate genes that drive cell cycle arrest, DNA repair, senescence, and apoptosis. Through this program, p53 prevents the propagation of damaged or potentially malignant cells. TP53 is the most frequently mutated gene in human cancer, and loss of p53 function compromises these protective responses. Because of its central role, p53 transcriptional activity is widely monitored in studies of genotoxic stress, apoptosis, and tumor suppression.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe P53 Reporter Lentivirus is a transcription factor reporter system that provides a sensitive fluorescent or luminescent readout of p53 activity in human or mouse cells. Tandem consensus p53 response elements drive expression of a reporter (GFP, RFP, firefly luciferase, or Renilla luciferase), so that p53 activation produces a quantitative signal indicative of p53 and apoptosis pathway engagement in transduced cells. Antibiotic selection markers (puromycin or blasticidin) support establishment of stable reporter cell lines. The system is used to study genotoxic stress responses, apoptosis, and tumor suppressor signaling, and to screen modulators of p53 activity. Supplied as lentiviral particles purified by PEG precipitation and sucrose gradient centrifugation, it efficiently transduces difficult-to-transfect cells, including primary and thawed cells.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis reporter lentivirus places a Firefly Luc, GFP, Luc, Renilla Luc, RFP reporter gene under the control of tandem consensus response elements specific for the Apoptosis\/p53 signaling pathway transcription factor, coupled to a minimal TATA-box promoter and a proprietary upstream enhancer that maximizes signal-to-noise. The constitutively expressed selection marker (Blasticidin, Puromycin) and\/or secondary reporter enables stable polyclonal cell line generation and flexible readout by fluorescence microscopy, flow cytometry, or luminometry.\u003c\/p\u003e\n\u003cp\u003eStable integration via the lentiviral backbone ensures consistent, clonally representative reporter expression in dividing and post-mitotic target cells — including primary T cells, macrophages, organoids, and cryopreserved material — eliminating the variability inherent to transient transfection. The self-inactivating LTR design and third-generation packaging minimize insertional mutagenesis risk and ensure biosafety classification at BSL-2.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"GFP \/ Puromycin \/ 5x10^6","offer_id":53251615621485,"sku":"LTV-0008-1S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Blasticidin \/ 5x10^6","offer_id":53310893982061,"sku":"LTV-0008-2S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Firefly Luc \/ Puromycin \/ 2x10^6","offer_id":53310894014829,"sku":"LTV-0008-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Firefly Luc \/ Blasticidin \/ 2x10^6","offer_id":53310894047597,"sku":"LTV-0008-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Puromycin \/ 5x10^6","offer_id":53310894080365,"sku":"LTV-0008-6S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Renilla Luc \/ Blasticidin \/ 2x10^6","offer_id":53310894113133,"sku":"LTV-0008-4SIC","price":595.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0949\/7424\/7277\/files\/TF-Reporter-Vector-circular_b476d082-2641-436d-80a2-b5c8f467b270.jpg?v=1776934151"},{"product_id":"kras-wild-type-and-mutant-orf-cdna-lentivirus-bhv19400100","title":"KRAS (Wild Type and Mutant) ORF cDNA Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eKRAS is a proto-oncogene encoding a small GTPase that acts as a molecular switch in growth-factor signaling. Cycling between an active GTP-bound and inactive GDP-bound state, KRAS relays signals from receptor tyrosine kinases to downstream effectors, principally the RAF-MEK-ERK and PI3K-AKT pathways, controlling cell proliferation, differentiation, and survival. Oncogenic point mutations, most commonly at codons 12, 13, and 61, lock KRAS in the active GTP-bound state, producing constitutive signaling. Such mutations are among the most frequent in human cancer, occurring at high rates in pancreatic, colorectal, and lung adenocarcinomas, and drive tumor initiation and progression. KRAS is therefore a central focus of cancer biology and targeted-therapy research.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe KRAS (Wild Type and Mutant) ORF cDNA Lentivirus delivers the human KRAS open reading frame (transcript variant a) for stable overexpression in mammalian cells, available as wild type or as common oncogenic mutants. An EF1a promoter drives expression of KRAS fused to a C-terminal V5 tag, linked via self-cleaving peptides to a fluorescent reporter (GFP or RFP) or firefly luciferase and a drug-selection marker (puromycin or blasticidin); in some constructs a PGK promoter drives the reporter and selection cassette separately. The lentiviral vectors are optimized for high expression and reliable genome integration, and the particles efficiently transduce difficult-to-transfect cells, including primary and thawed cultures, supporting stable cell line generation for studies of RAS signaling and oncogenic transformation. ORF integrity is verified by sequencing and expression confirmed by transient transfection.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis ORF cDNA lentivirus enables stable overexpression of KRAS (NCBI Accession: NM_033360) in mammalian cells via a third-generation, VSV-G pseudotyped delivery system. The ORF cDNA is fused to a C-terminal epitope tag (V5, Myc, or HA) and expressed under a strong constitutive promoter (EF1a). Reporter and selection marker components (Firefly Luciferase, GFP, RFP; Blasticidin, Puromycin) are co-expressed via self-cleaving P2A peptides, enabling independent protein production without fusion-tag artifacts.\u003c\/p\u003e\n\u003cp\u003eUltra-purification by PEG precipitation and sucrose gradient centrifugation yields high-titer particles suitable for primary cells, suspension cultures, and stem cells. Stable polyclonal cell lines are established within 10–14 days by antibiotic selection or FACS sorting. For in vivo applications, the serum-free formulation and VSV-G envelope support direct administration or further concentration for stereotactic injection.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"EF1a-KRAS-G12C-Flag \/ none\/Puromycin \/ 3x10^6","offer_id":53251618537837,"sku":"LCV-0008-11-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-V5 \/ GFP\/none \/ 3x10^6","offer_id":53311256854893,"sku":"LCV-0008-1S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-G12V-Flag \/ none\/Blasticidin \/ 3x10^6","offer_id":53311256887661,"sku":"LCV-0008-10-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-G12D-V5 \/ Firefly Luciferase\/none \/ 2x10^6","offer_id":53311256920429,"sku":"LCV-0008-09-5","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-G12V-Flag \/ none\/Puromycin \/ 3x10^6","offer_id":53311256953197,"sku":"LCV-0008-10-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-Flag \/ none\/Puromycin \/ 3x10^6","offer_id":53311256985965,"sku":"LCV-0008-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-G12D-Flag \/ none\/Blasticidin \/ 3x10^6","offer_id":53311257018733,"sku":"LCV-0008-09-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-G12D-Flag \/ none\/Puromycin \/ 3x10^6","offer_id":53311257051501,"sku":"LCV-0008-09-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-G12C-Flag \/ none\/Blasticidin \/ 3x10^6","offer_id":53311257084269,"sku":"LCV-0008-11-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-V5 \/ RFP\/none \/ 3x10^6","offer_id":53311257117037,"sku":"LCV-0008-2S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"EF1a-KRAS-Flag \/ none\/Blasticidin \/ 3x10^6","offer_id":53311257149805,"sku":"LCV-0008-4S","price":595.0,"currency_code":"USD","in_stock":true}]},{"product_id":"sre-reporter-lentivirus-bhv19400024","title":"SRE Reporter Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe serum response element (SRE) is a promoter motif that mediates transcriptional responses to growth factor and mitogen signaling, classically studied in the c-Fos promoter. The SRE is bound by serum response factor (SRF) together with ternary complex factors such as ELK-1. Growth factor stimulation activates the MAPK\/ERK cascade, leading to ERK1\/2 (MAPK3\/MAPK1)-mediated phosphorylation of ELK-1, which together with SRF drives rapid induction of immediate-early genes. This pathway controls cell proliferation, differentiation, and survival, and its dysregulation is implicated in cancer and other proliferative disorders, making SRE-driven reporters valuable for monitoring MAPK\/ERK and growth factor signaling.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe SRE Reporter Lentivirus places a reporter gene under the control of tandem c-Fos serum response elements, providing a sensitive readout of MAPK\/ERK and growth factor signaling through serum response factor and its cofactors, including ELK-1. Reporter options include fluorescent (GFP, RFP), luminescent (firefly and Renilla luciferase), and combined GFP\/Luc and RFP\/Luc formats, with blasticidin or puromycin selection for stable reporter cell line establishment.\u003c\/p\u003e\n\u003cp\u003eThe particles are purified by PEG precipitation and sucrose gradient centrifugation and efficiently transduce difficult-to-transfect cells, including primary and cryopreserved cultures. Applications include monitoring MAPK\/ERK pathway activation, studying mitogen and growth factor responses, and screening modulators of this signaling axis.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis reporter lentivirus places a Firefly Luc, GFP, GFP\/Luc, Luc, Renilla Luc, RFP, RFP\/Luc reporter gene under the control of tandem consensus response elements specific for the MAPK\/ERK pathway transcription factor, coupled to a minimal TATA-box promoter and a proprietary upstream enhancer that maximizes signal-to-noise. The constitutively expressed selection marker (Blasticidin, Puromycin) and\/or secondary reporter enables stable polyclonal cell line generation and flexible readout by fluorescence microscopy, flow cytometry, or luminometry.\u003c\/p\u003e\n\u003cp\u003eStable integration via the lentiviral backbone ensures consistent, clonally representative reporter expression in dividing and post-mitotic target cells — including primary T cells, macrophages, organoids, and cryopreserved material — eliminating the variability inherent to transient transfection. The self-inactivating LTR design and third-generation packaging minimize insertional mutagenesis risk and ensure biosafety classification at BSL-2.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"GFP \/ Puromycin \/ 5x10^6","offer_id":53251619455341,"sku":"LTV-0028-1S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Blasticidin \/ 5x10^6","offer_id":53310898962797,"sku":"LTV-0028-2S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Firefly Luc \/ Puromycin \/ 2x10^6","offer_id":53310898995565,"sku":"LTV-0028-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Firefly Luc \/ Blasticidin \/ 2x10^6","offer_id":53310899028333,"sku":"LTV-0028-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"GFP \/ Blasticidin \/ 5x10^6","offer_id":53310899061101,"sku":"LTV-0028-5S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Puromycin \/ 5x10^6","offer_id":53310899093869,"sku":"LTV-0028-6S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Renilla Luc \/ Blasticidin \/ 2x10^6","offer_id":53310899126637,"sku":"LTV-0028-4SIC","price":595.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0949\/7424\/7277\/files\/LTV-0028-SRE-TAG-Puro-Fig.-2-FBS-treatment.jpg?v=1776934451"},{"product_id":"rre-reporter-lentivirus-bhv19400242","title":"RRE Reporter Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe RAS-ERK pathway is a central signaling cascade in which growth factor activation of RAS GTPases drives the RAF-MEK-ERK kinase module, ultimately altering gene transcription that governs cell proliferation, differentiation, and survival. Activated ERK regulates transcription factors that bind the Ras-responsive element (RRE), including ETS family members such as ERG, ETV1, ETV4, and ETV5, as well as RREB-1. These factors mediate the gene expression changes associated with oncogenic transformation. Aberrant RAS-ERK signaling, whether through RAS mutation or ETS gene rearrangement, is a frequent driver of human cancers, making RRE-dependent transcription an informative readout of pathway activity and a target for inhibitor discovery.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe RRE Reporter Lentivirus is a transcription-factor reporter system designed to detect transcription downstream of RAS-ERK signaling. The construct contains tandem repeats of the Ras-responsive element coupled to a minimal promoter, driving a fluorescent or luminescent reporter chosen from options including GFP, RFP, mCherry, BFP2, firefly luciferase, Gaussia luciferase, and dual configurations. A constitutively expressed selection marker supports stable polyclonal cell line generation, with readout by microscopy, flow cytometry, or luminometry.\u003c\/p\u003e\n\u003cp\u003eThe system is suited to monitoring RAS-ERK pathway activation, screening pathway inhibitors, and studying oncogenic signaling driven by ETS family transcription factors and RREB-1. Particles are purified by PEG precipitation and sucrose gradient centrifugation for effective transduction of primary and thawed cells.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis reporter lentivirus places a BFP2, d2GFP, EGFP, Firefly Luc, Gaussia Luc, GFP, GFP + Firefly Luc, mCherry, Renilla Luc, RFP, RFP + Firefly Luc reporter gene under the control of tandem consensus response elements specific for the RAS-ERK Pathway transcription factor, coupled to a minimal TATA-box promoter and a proprietary upstream enhancer that maximizes signal-to-noise. The constitutively expressed selection marker (Blasticidin, Hygromycin, Puromycin, Zeocin) and\/or secondary reporter enables stable polyclonal cell line generation and flexible readout by fluorescence microscopy, flow cytometry, or luminometry.\u003c\/p\u003e\n\u003cp\u003eStable integration via the lentiviral backbone ensures consistent, clonally representative reporter expression in dividing and post-mitotic target cells — including primary T cells, macrophages, organoids, and cryopreserved material — eliminating the variability inherent to transient transfection. The self-inactivating LTR design and third-generation packaging minimize insertional mutagenesis risk and ensure biosafety classification at BSL-2.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"RRE-TAG-Puro \/ GFP \/ 5x10^6","offer_id":53251624993133,"sku":"LTV-0135-1S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Negative Control (NC-TAG-Puro) \/ GFP \/ 5x10^6","offer_id":53362087428461,"sku":"LTV-0135-1N","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Positive Control (PC-TAG-Puro) \/ GFP \/ 5x10^6","offer_id":53362087461229,"sku":"LTV-0135-1P","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RRE-TAL-Puro \/ Firefly Luc \/ 2x10^6","offer_id":53362087493997,"sku":"LTV-0135-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Negative Control (NC-TAL-Puro) \/ Firefly Luc \/ 2x10^6","offer_id":53362087526765,"sku":"LTV-0135-3N","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Positive Control (PC-TAL-Puro) \/ Firefly Luc \/ 2x10^6","offer_id":53362087559533,"sku":"LTV-0135-3P","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Internal Control (RLuc-BSD) \/ Renilla Luc \/ 2x10^6","offer_id":53362087592301,"sku":"LTV-0135-3R","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RRE-TAR-BSD \/ RFP \/ 5x10^6","offer_id":53362087625069,"sku":"LTV-0135-2S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RRE-TAL-BSD \/ Firefly Luc \/ 2x10^6","offer_id":53362087657837,"sku":"LTV-0135-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RRE-TAG-BSD \/ GFP \/ 5x10^6","offer_id":53362087690605,"sku":"LTV-0135-5S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RRE-TAR-Puro \/ RFP \/ 5x10^6","offer_id":53362087723373,"sku":"LTV-0135-6S","price":595.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0949\/7424\/7277\/files\/rre.jpg?v=1776934141"},{"product_id":"h-m-p53-shrna-lentivirus-bhv19400149","title":"h\/m P53 shRNA Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003ep53, encoded by TP53, is a transcription factor and one of the most important tumor suppressors in the cell. In response to DNA damage, oncogene activation, and other stresses, p53 is stabilized and activates programs of cell cycle arrest, DNA repair, senescence, and apoptosis to prevent the propagation of damaged cells. p53 also regulates metabolism, autophagy, and ferroptosis. TP53 is the most frequently mutated gene in human cancer, and loss of p53 function permits genomic instability and uncontrolled proliferation. Because of its central role in guarding genome integrity, p53 is a major focus of cancer research.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe h\/m P53 shRNA Lentivirus delivers validated short hairpin RNA targeting human and mouse TP53 from a third-generation, self-inactivating lentiviral backbone. shRNA expression is driven by a U6 promoter, with a co-expressed fluorescent reporter (GFP or RFP) and antibiotic selection marker. VSV-G pseudotyping enables broad tropism across primary, suspension, and cryopreserved cells, and each shRNA is validated for at least 70% p53 knockdown by a fluorescence-based method.\u003c\/p\u003e\n\u003cp\u003eHigh-titer particles are ultra-purified by PEG precipitation and sucrose gradient centrifugation. A shRNA set option provides a mix of two independent validated shRNAs plus a scrambled control. Applications include loss-of-function studies of tumor suppression, the DNA damage response, cell cycle control, and apoptosis.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis validated shRNA lentivirus targeting TP53 (NCBI Accession: NM_000546.6) delivers a 19–20 bp shRNA from a third-generation, self-inactivating lentiviral backbone. Expression is driven from a U6 Pol III promoter, with a constitutively expressed fluorescent reporter (GFP, GFP\/Luc, RFP, RFP\/Luc) and antibiotic selection marker (Puromycin, Blasticidin) co-expressed from the same vector. VSV-G pseudotyping enables broad cell tropism, including primary, suspension, and cryopreserved cell types.\u003c\/p\u003e\n\u003cp\u003eKnockdown is validated using a proprietary bicistronic fluorescence assay in which the target mRNA is co-expressed fused to RFP alongside the shRNA-GFP construct. At least 70% reduction in RFP signal in GFP-positive cells confirms on-target activity — a more direct functional readout than transcript-level qPCR. Polyclonal stable lines can be generated by antibiotic selection within 10 days, preserving parental cell heterogeneity compared to single-clone CRISPR approaches.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"None \/ Blasticidin \/ 2x10^6","offer_id":53251625124205,"sku":"LSV-0034-T2","price":1195.0,"currency_code":"USD","in_stock":true},{"title":"None \/ Puromycin \/ 2x10^6","offer_id":53311259312493,"sku":"LSV-0034-T1","price":1195.0,"currency_code":"USD","in_stock":true},{"title":"GFP \/ Puromycin \/ 5x10^6 (sh-mix) + 5x10^6 (scr-mix)","offer_id":53311259345261,"sku":"LSV-0034-SET1","price":1195.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Blasticidin \/ 5x10^6 (sh-mix) + 5x10^6 (scr-mix)","offer_id":53311259378029,"sku":"LSV-0034-SET2","price":1195.0,"currency_code":"USD","in_stock":true},{"title":"GFP \/ Puromycin \/ 5x10^6","offer_id":53311259410797,"sku":"LSV-0034-1S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Blasticidin \/ 5x10^6","offer_id":53311259443565,"sku":"LSV-0034-2S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"GFP\/Luc \/ None \/ 2x10^6","offer_id":53311259476333,"sku":"LSV-0034-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP\/Luc \/ None \/ 2x10^6","offer_id":53311259509101,"sku":"LSV-0034-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"GFP \/ Blasticidin \/ 5x10^6","offer_id":53311259541869,"sku":"LSV-0034-5S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Puromycin \/ 5x10^6","offer_id":53311259574637,"sku":"LSV-0034-6S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"None \/ Puromycin \/ 5x10^6","offer_id":53311259607405,"sku":"LSV-0034-7S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"None \/ Blasticidin \/ 5x10^6","offer_id":53311259640173,"sku":"LSV-0034-8S","price":595.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0949\/7424\/7277\/files\/LSV-0034-h-P53-sh-fig1.jpg?v=1776934281"},{"product_id":"h-m-wnt16-shrna-lentivirus-bhv19400208","title":"h\/m WNT16 shRNA Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eWNT16 (Wnt Family Member 16) is a secreted glycoprotein of the Wnt family of signaling ligands that act through Frizzled receptors to regulate both canonical (β-catenin-dependent) and non-canonical Wnt pathways. WNT16 is a notable regulator of bone mass and skeletal homeostasis, influencing cortical bone thickness, osteoblast and osteoclast activity, and fracture susceptibility, and has been identified in genome-wide studies of bone mineral density. Wnt signaling more broadly controls cell proliferation, differentiation, and tissue patterning, and its dysregulation contributes to skeletal disorders and cancer, making WNT16 a relevant target for bone biology and oncology research.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe h\/m WNT16 shRNA Lentivirus provides high-titer lentiviral particles for stable knockdown of human and mouse WNT16. The shRNA is delivered from a third-generation, self-inactivating backbone with expression from a U6 Pol III promoter, alongside a constitutively expressed fluorescent reporter (GFP or RFP, optionally with luciferase) and an antibiotic selection marker. VSV-G pseudotyping enables broad tropism, including primary, suspension, and cryopreserved cells. The shRNA is validated to achieve at least 70% knockdown using a fluorescence-based assay. The set comprises lentivirus produced from a mix of two independent validated shRNAs plus a matched scrambled-shRNA control. It is used to study WNT16 loss of function in Wnt signaling, bone biology, and cancer research.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis validated shRNA lentivirus targeting WNT16 delivers a 19–20 bp shRNA from a third-generation, self-inactivating lentiviral backbone. Expression is driven from a U6 Pol III promoter, with a constitutively expressed fluorescent reporter (GFP, GFP\/Luc, RFP, RFP\/Luc) and antibiotic selection marker (Blasticidin, Puromycin) co-expressed from the same vector. VSV-G pseudotyping enables broad cell tropism, including primary, suspension, and cryopreserved cell types.\u003c\/p\u003e\n\u003cp\u003eKnockdown is validated using a proprietary bicistronic fluorescence assay in which the target mRNA is co-expressed fused to RFP alongside the shRNA-GFP construct. At least 70% reduction in RFP signal in GFP-positive cells confirms on-target activity — a more direct functional readout than transcript-level qPCR. Polyclonal stable lines can be generated by antibiotic selection within 10 days, preserving parental cell heterogeneity compared to single-clone CRISPR approaches.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"GFP \/ Puromycin \/ 5x10^6 (sh-mix) + 5x10^6 (scr-mix)","offer_id":53251625484653,"sku":"LSV-0063-SET1","price":1195.0,"currency_code":"USD","in_stock":true},{"title":"GFP \/ Puromycin \/ 5x10^6","offer_id":53362029330797,"sku":"LSV-0063-1S","price":595.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0949\/7424\/7277\/files\/hm-WNT16-shRNA-Figure.jpg?v=1776934211"},{"product_id":"tcf-lef-reporter-lentivirus-bhv19400010","title":"TCF\/LEF Reporter Lentivirus","description":"\u003cdiv class=\"bhp-desc\"\u003e\n\u003cstyle\u003e.bhp-desc{font-size:16px;color:#1a1a1a;line-height:1.7}.bhp-desc h2{font-size:18px;font-weight:700;color:#003366;margin:24px 0 10px;padding-bottom:6px;border-bottom:2px solid #003366}.bhp-desc p{margin:0 0 12px}.bhp-desc ul{margin:0 0 12px 22px}.bhp-desc li{margin:0 0 6px}\u003c\/style\u003e\n\u003ch2\u003e\u003cstrong\u003eBackground\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eTCF\/LEF transcription factors, including TCF7, LEF1, and TCF7L2, are the nuclear effectors of the canonical Wnt signaling pathway. In the absence of Wnt ligand, beta-catenin is continuously degraded and TCF\/LEF factors repress target genes. When Wnt signaling is active, beta-catenin is stabilized, accumulates in the nucleus, and partners with TCF\/LEF proteins at Wnt response elements to activate transcription. This pathway governs cell proliferation, fate determination, stem cell maintenance, and tissue patterning during development and homeostasis. Aberrant activation of Wnt\/beta-catenin signaling, often through mutations affecting beta-catenin or its regulators, is a major driver of colorectal and other cancers, making this pathway a central focus of developmental biology and cancer research.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eProduct Description \u0026amp; Applications\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThe TCF\/LEF Reporter Lentivirus is a TOPFlash-style transcription factor reporter system that provides a fluorescent or luminescent readout of Wnt\/beta-catenin pathway activation in mammalian cells. The construct places a reporter gene (d2GFP, GFP, RFP, firefly luciferase, or Renilla luciferase) under the control of tandem Wnt response elements coupled to a minimal promoter and an optimized upstream enhancer that maximizes signal-to-noise. Reporter activity is driven primarily by LEF1, with contributions from TCF1 and context-dependent TCF4. A constitutive drug selection marker (Blasticidin or Puromycin) enables generation of stable polyclonal reporter cell lines. Supplied as high-titer particles purified by PEG precipitation and sucrose gradient centrifugation, it is well suited to studying Wnt\/beta-catenin signaling in primary and difficult-to-transfect cells.\u003c\/p\u003e\n\u003ch2\u003e\u003cstrong\u003eAbout This Product\u003c\/strong\u003e\u003c\/h2\u003e\n\u003cp\u003eThis reporter lentivirus places a d2GFP, Firefly Luc, GFP, Luc, Renilla Luc, RFP reporter gene under the control of tandem consensus response elements specific for the Wnt\/b-catenin pathway transcription factor, coupled to a minimal TATA-box promoter and a proprietary upstream enhancer that maximizes signal-to-noise. The constitutively expressed selection marker (Blasticidin, Puromycin) and\/or secondary reporter enables stable polyclonal cell line generation and flexible readout by fluorescence microscopy, flow cytometry, or luminometry.\u003c\/p\u003e\n\u003cp\u003eStable integration via the lentiviral backbone ensures consistent, clonally representative reporter expression in dividing and post-mitotic target cells — including primary T cells, macrophages, organoids, and cryopreserved material — eliminating the variability inherent to transient transfection. The self-inactivating LTR design and third-generation packaging minimize insertional mutagenesis risk and ensure biosafety classification at BSL-2.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"LipExoGen Biotech","offers":[{"title":"GFP \/ Puromycin \/ 5x10^6","offer_id":53251625386349,"sku":"LTV-0011-1S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Blasticidin \/ 5x10^6","offer_id":53310902698349,"sku":"LTV-0011-2S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Firefly Luc \/ Puromycin \/ 2x10^6","offer_id":53310902731117,"sku":"LTV-0011-3S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Firefly Luc \/ Blasticidin \/ 2x10^6","offer_id":53310902763885,"sku":"LTV-0011-4S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"GFP \/ Blasticidin \/ 5x10^6","offer_id":53310902796653,"sku":"LTV-0011-5S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"RFP \/ Puromycin \/ 5x10^6","offer_id":53310902829421,"sku":"LTV-0011-6S","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Selection-Puromycin \/ Puromycin \/ 5x10^6","offer_id":53310902862189,"sku":"LTV-0011-1D2","price":595.0,"currency_code":"USD","in_stock":true},{"title":"Selection-Puromycin \/ Puromycin \/ 2x10^6","offer_id":53310902894957,"sku":"LTV-0011-1SMT","price":595.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0949\/7424\/7277\/files\/TOPFlash-HEK-reporter-2.jpg?v=1776934150"},{"product_id":"crma-adenovirus-ad-cmv-crma-bhv21600014","title":"CrmA Adenovirus (Ad-CMV-CrmA)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-CrmA is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the CrmA gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e CrmA.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eCytokine response modifier A\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Caspase Inhibitors.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1032-crma-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487720301,"sku":"1032","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"apc-adenovirus-ad-cbr-bhv21600044","title":"APC Adenovirus (Ad-CBR)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CBR is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the CBR gene with a eGFP epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e CBR (eGFP tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eAdenomatous polyposis coli gene (APC) is a tumor suppressor gene located on chromosome 5q2. It is inactivated in most colorectal tumors. APC is a cytoplasmic protein that can bind to and promote the degradation of b-catenin. In most colorectal tumors, APC is inactivated. This increases the interaction between b-catenin and Tcf family of transcription factors, leading to increase transcription of genes such as c-Myc.\u003c\/p\u003e\u003cp\u003eThis adenovirus contains APC mini-me fragment.\u003c\/p\u003e\u003cp\u003eShih IM., et al., Cancer Res. 2000 Mar 15;60(6):1671-6.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying TGF-β \/ WNT.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1283-apc-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487851373,"sku":"1283","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"akt1-adenovirus-ad-cmv-akt1-wt-bhv21600004","title":"Akt1 Adenovirus (Ad-CMV-Akt1 (wt))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Akt1 (wt) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Akt1 (wt) gene with a HA epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Akt1 (wt) (HA tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eAn HA tag was fused in frame to the N termini of the mouse Akt1 coding sequences.\u003c\/p\u003e\u003cp\u003eAkt1\/PKB is activated in response to many extracellular signals and play key roles in regulating diverse cellular processes, including cell proliferation, differentiation, apoptosis, angiogenesis and glycogen synthesis etc. Akt1 is activated by the phosphorylation of the T loop of their kinase domain by PDK1 and by phosphorylation of a residue located C-terminal to the kinase domain in the hydrophobic motif.\u003c\/p\u003e\u003cp\u003eThe Akt family of kinases includes Akt1, Akt2 and Akt3.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1022-akt1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487916909,"sku":"1022","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"akt2-myr-adenovirus-ad-cmv-akt2-myr-bhv21600005","title":"Akt2 (Myr) Adenovirus (Ad-CMV-Akt2 (Myr))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Akt2 (Myr) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Akt2 (Myr) gene with a HA epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Akt2 (Myr) (HA tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eHA-Akt2 is constructed by fusing the HA tag in frame to the N termini of the coding sequence of wild type Akt2. To construct Myr-HA-Akt2, the c-Src myristoylation sequence was fused in frame to the N terminus of the HA-Akt2 (wild-type) coding sequence. Myr-HA-Akt2 is a constitutively active mutant of Akt2, and it is also referred as Akt2(ca).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1023-akt2-myr-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487949677,"sku":"1023","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"akt1-dn-adenovirus-ad-cmv-akt1-dn-bhv21600003","title":"Akt1 (dn) Adenovirus (Ad-CMV-Akt1 (dn))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Akt1 (dn) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Akt1 (dn) gene with a HA epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Akt1 (dn) (HA tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eAn HA tag was fused in frame to the N termini of the coding sequence of mouse Akt1(T308A, S473A) mutant, which is also known as Akt1(AA).\u003c\/p\u003e\u003cp\u003eAkt1\/PKB is activated in response to many extracellular signals and play key roles in regulating diverse cellular processes, including cell proliferation, differentiation, apoptosis, angiogenesis and glycogen synthesis etc. Akt1 is activated by the phosphorylation of the T loop of their kinase domain by PDK1 and by phosphorylation of a residue located C-terminal to the kinase domain in the hydrophobic motif.\u003c\/p\u003e\u003cp\u003eThe Akt family of kinases includes Akt1, Akt2 and Akt3.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1021-akt1-dn-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487982445,"sku":"1021","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"akt1myr-adenovirus-ad-cmv-akt1-myr-bhv21600002","title":"Akt1(Myr) Adenovirus (Ad-CMV-Akt1 (Myr))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Akt1 (Myr) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Akt1 (Myr) gene with a HA epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Akt1 (Myr) (HA tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eHA-Akt1 is constructed by fusing the HA tag in frame to the N termini of the coding sequence of wild type Akt1. To construct Myr-HA-Akt1, the c-Src myristoylation sequence was fused in frame to the N terminus of the HA-Akt (wild-type) coding sequence. Myr-HA-Akt1 is a constitutively active mutant of Akt1, and it is also referred as Akt(ca).\u003c\/p\u003e\u003cp\u003eAkt1\/PKB is activated in response to many extracellular signals and play key roles in regulating diverse cellular processes, including cell proliferation, differentiation, apoptosis, angiogenesis and glycogen synthesis etc. Akt1 is activated by the phosphorylation of the T loop of their kinase domain by PDK1 and by phosphorylation of a residue located C-terminal to the kinase domain in the hydrophobic motif.\u003c\/p\u003e\u003cp\u003eThe Akt family of kinases includes Akt1, Akt2 and Akt3.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1020-akt1myr-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488146285,"sku":"1020","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"c-ras-adenovirus-ad-cmv-c-ras-bhv21600012","title":"c-Ras Adenovirus (Ad-CMV-c-Ras)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-c-Ras is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the c-Ras gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e c-Ras.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ec-Ras is delivered to target cells via adenoviral transduction. Adenoviral delivery results in episomal (non-integrating) expression with rapid onset (typically detectable by 24 hours, peaking at 48–72 hours).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying RAS\/RAF\/MEK\/ERK Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1030-c-ras-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488211821,"sku":"1030","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"akt2-adenovirus-ad-cmv-akt2-wt-bhv21600006","title":"Akt2 Adenovirus (Ad-CMV-Akt2 (wt))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Akt2 (wt) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Akt2 (wt) gene with a HA epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Akt2 (wt) (HA tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe Akt family of kinases includes Akt1, Akt2 and Akt3.\u003c\/p\u003e\u003cp\u003eAn HA tag was fused in frame to the N termini of the mouse Akt2 coding sequences.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1024-akt2-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488277357,"sku":"1024","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"ras-n17-adenovirus-ad-cmv-ras-n17-bhv21600013","title":"Ras (N17) Adenovirus (Ad-CMV-Ras (N17))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Ras (N17) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Ras (N17) gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Ras (N17).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eRas genes encode 21 kDa guanine nucleotide-binding proteins, including H-, K- and N-Ras. H-Ras was first identified as oncogene, mutated Ras genes have been found in many human tumors. Like all GTPases, Ras act as molecular switch to control downstream cellular events. The interconversion of the inactive GDP-bound form into the active GTP-bound form is regulated by guanine nucleotide exchange factors, whereas inactivation of the GTP-bound form is stimulated by GTPase-activating proteins (GAPs). Ras in its active GTP bound form binds to Raf, resulting in activation of MAP kinase cascade. The provided recombinant adenovirus contains dominant negative form of human H-Ras (T17N).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying RAS\/RAF\/MEK\/ERK Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1031-ras-n17-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488310125,"sku":"1031","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"c-myc-adenovirus-ad-c-myc-bhv21600046","title":"c-Myc Adenovirus (Ad-c-Myc)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-c-Myc is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the c-Myc gene with a eGFP epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e c-Myc (eGFP tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ec-Myc is a very strong proto-oncogene and it is very often found to be upregulated in many types of cancers. It is a mammalian transcription factor belonging to the bHLH (basic Helix Loop Helix)-Leucine Zipper family. The Myc family of cellular oncogenes, which includes c-Myc, N-Myc, L-Myc, S-Myc and B-Myc, represents nuclear transcription factors that play a significant role in cellular proliferation, differentiation, apoptosis and transformation. Members of this gene family are activated upon various mitogenic signals such as Wnt, Shh and EGF. They form heteromeric complexes with other interacting partners, such as members of the Max and Mad families, to activate transcription. Alternatively, c-Myc can also inhibit the DNA binding protein Miz-1 to repress a second set of target genes. Mnt and Mlx regulate Myc activity by forming heterodimers with Max or Mad, respectively, to suppress Myc-induced transcriptional activation.\u003c\/p\u003e\u003cp\u003eThis adenovirus contain human c-Myc. It was constructed using AdEasy system.\u003c\/p\u003e\u003cp\u003eReference: Hermeking H., et al., Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2229-34.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying MYC Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1285-c-myc-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488441197,"sku":"1285","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"fas-ligand-adenovirus-ad-cmv-fasl-bhv21600011","title":"Fas Ligand Adenovirus (Ad-CMV-FasL)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-FasL is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the FasL gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e FasL.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThis catalog number has been changed to #1594. Please go to the product page for cat#1594 for detail.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Death Receptors.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1029-fas-ligand-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488506733,"sku":"1029","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"fas-ligand-tet-on-adenovirus-ad-tet-on-fasl-bhv21600037","title":"Fas Ligand (tet-on) Adenovirus (Ad-Tet-on-FasL)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-Tet-on-FasL is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the on-FasL gene under the Tet-on promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (Tet-on):\u003c\/strong\u003e a doxycycline-inducible promoter system requiring tetracycline transactivator co-expression.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e on-FasL.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe FasL transgene is under the control of a tetracycline-regulated promoter.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Death Receptors.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1200-fas-ligand-tet-on-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488539501,"sku":"1200","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"brca1-adenovirus-ad-brca1-bhv21600054","title":"BRCA1 Adenovirus (Ad-BRCA1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-BRCA1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the BRCA1 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e BRCA1.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe breast cancer susceptibility gene, BRCA1, which maps to chromosome 17q is expressed in numerous tissues, including breast and ovary. A second breast cancer susceptibility gene, BRCA2, located on chromosome 13q12-13, also confers a high incidence of breast and ovarian cancer. Mutations within the BRCA1 gene may account for at least 80% of families with increased incidence of both early-onset breast cancer and ovarian cancer.\u003c\/p\u003e\u003cp\u003eThis adenovirus expresses the human BRCA1 transcript variant 5 (NM_007299).  This variant differs in the 5′ UTR, uses two alternate in-frame splice sites in the central coding region, and lacks an alternate exon in the 3′ coding region that results in a frameshift, compared to variant 1. So this variant is shorter and has a distinct C-terminus, compared to BRCA1 isoform 1.\u003c\/p\u003e\u003cp\u003ePlease contact us if you need adenoviruses expressing other isoforms of human BRCA1.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying DNA Repair.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1351-brca1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488572269,"sku":"1351","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"rb-adenovirus-ad-cmv-rb-bhv21600018","title":"Rb Adenovirus (Ad-CMV-Rb)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Rb is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Rb gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Rb.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe retinoblastoma susceptibility protein Rb is a 110 kDa phosphorylated protein. Like p53, Rb p110 is an anti-oncogene that is subject to inactivation by either mutation or by binding to certain DNA tumor virus-encoded proteins. Rb binds to and regulates transcription factors involved in cell cycle regulation, including the E2F family. Two Rb related proteins, p107 and p130, also function to regulate specific members of the E2F transcription factor family. Binding and inactivation of E2F proteins by Rb is regulated by cyclin dependent kinase-mediated phosphorylation\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Rb \/ Cell Cycle.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1043-rb-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488605037,"sku":"1043","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"p53-adenovirus-ad-p53-gfp-bhv21600040","title":"p53 Adenovirus (Ad-p53-GFP)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-p53-GFP is a replication-defective recombinant Ad5 adenovirus expressing the GFP reporter gene under the p53 promoter. Reporter adenoviruses are commonly used to benchmark transduction efficiency, titrate MOI in new cell or animal models, and as transduction-load controls for paired over-expression vectors.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (p53):\u003c\/strong\u003e a p53-responsive promoter element.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e GFP (eGFP tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe widely studied p53 tumor suppressor gene contains mutations in over 50% of human cancers. p53 protein expression is low in normal cells but increases in response to DNA damage and cellular distress signals. Overexpression of the p53 transcription factor can induce either cell cycle arrest or apoptosis through transcriptional regulation of several genes, including the cell cycle inhibitor p21, DNA repair gene GADD45 and the apoptotic inducer Bax. p53 also induces apoptosis by means of a direct signaling pathway involving the expression of p53AIP1. p53 directly binds to and acts on several cellular proteins involved in various pathways, including c-Abl, basal transcription factor TFIIH and WT1. p53 can be functionally inactivated by mutation, binding to DNA tumor virus encoded proteins, such as SV40 large T antigen, Adenovirus E1B and papilloma virus E6 proteins, or through its interaction with MDM2.\u003c\/p\u003e\u003cp\u003eThis adenovirus express both human p53 and GFP.\u003c\/p\u003e\u003cp\u003eReference: Yu J., et al., PNAS (1999) 96: 14517; Chan TA., et al., Genes Dev (00) 14:1584\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying p53 Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eTransduction-efficiency benchmarking in new cell lines or animal models.\u003c\/li\u003e\n\u003cli\u003eMOI titration as a positive control before switching to a transgene of interest.\u003c\/li\u003e\n\u003cli\u003ePromoter-activity readout for transcriptional studies.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1260-p53-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488899949,"sku":"1260","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"p21-cdkn1a-adenovirus-ad-cmv-p21-bhv21600016","title":"p21\/CDKN1A Adenovirus (Ad-CMV-p21)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-p21 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the p21 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e p21.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ep21\/CDKN1A is a cyclin-dependent kinase inhibitor. It is a key effector of cellular senescence downstream of the tumor suppressor p53. p21 binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of p21\/CDKN1A is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. P21 can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying CDK Inhibitors.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1041-p21-cdkn1a-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488965485,"sku":"1041","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"c-jun-dn-adenovirus-ad-cmv-c-jun-dn-bhv21600021","title":"c-JUN (dn) Adenovirus (Ad-CMV-c-JUN (DN))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-c-JUN (DN) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the c-JUN (DN) gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e c-JUN (DN).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThis recombinant adenovirus contains c-Jun (TAM67 mutant).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying AP-1 \/ Stress Response.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1046-c-jun-dn-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488932717,"sku":"1046","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"p53-adenovirus-ad-cmv-p53-bhv21600033","title":"p53 Adenovirus (Ad-CMV-p53)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-p53 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the p53 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e p53.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe widely studied p53 tumor suppressor gene contains mutations in over 50% of human cancers. p53 protein expression is low in normal cells but increases in response to DNA damage and cellular distress signals. Overexpression of the p53 transcription factor can induce either cell cycle arrest or apoptosis through transcriptional regulation of several genes, including the cell cycle inhibitor p21, DNA repair gene GADD45 and the apoptotic inducer Bax. p53 also induces apoptosis by means of a direct signaling pathway involving the expression of p53AIP1. p53 directly binds to and acts on several cellular proteins involved in various pathways, including c-Abl, basal transcription factor TFIIH and WT1. p53 can be functionally inactivated by mutation, binding to DNA tumor virus encoded proteins, such as SV40 large T antigen, Adenovirus E1B and papilloma virus E6 proteins, or through its interaction with MDM2.\u003c\/p\u003e\u003cp\u003eReference: Polyak K., et al., Genes Dev. 1996 Aug 1;10(15):1945-52.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying p53 Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1168-p53-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488998253,"sku":"1168","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"caspase-9-dn-adenovirus-ad-cmv-caspase-9-dn-bhv21600019","title":"Caspase 9 (dn) Adenovirus (Ad-CMV-Caspase 9 (DN))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Caspase 9 (DN) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Caspase 9 (DN) gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Caspase 9 (DN).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThis adenovirus contains a Caspase 9 (C287A mutant).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Caspase Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1044-caspase-9-dn-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489096557,"sku":"1044","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"phosphoinositide-3-kinase-adaptor-protein-1-adenovirus-ad-pi3kap1-bhv21600119","title":"Phosphoinositide-3-kinase adaptor protein 1 Adenovirus (Ad-PI3KAP1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PI3KAP1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PI3KAP1 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e PI3KAP1.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eB cell adaptor protein (BCAP), also known as phosphoinositide-3-kinase (PI3K) adaptor protein, is a protein tyrosine kinase substrate that couples B-cell receptor to PI3K activation. Tyrosine phosphorylation of BCAP is mediated by Syk and Btk, creating a binding site for PI3K. It is involved in the regulation of PI3K localization. BCAP is expressed in B-cell and macrophage cell-lines but also in various tissues such as spleen, lung, liver and thymus.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1421-phosphoinositide-3-kinase-adaptor-protein-1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489194861,"sku":"1421","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"t-cell-factor-4-adenovirus-ad-tcf4-bhv21600101","title":"T-cell factor 4 Adenovirus (Ad-TCF4)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-TCF4 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the TCF4 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e TCF4.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eT-cell factor (TCF-1) and lymphoid enhancer-binding factor (for LEF-1, also designated TCF-1?) compose a family of DNA-binding transcriptional activators that are essential for lymphoid cell development. These transcription factors are activated by the Wnt-1 and Wingless pathways and are characterized by the presence of a conserved protein motif, the high mobility group (HMG) 1 box, which mediates DNA binding. LEF-1, TCF-1, and two other family members, TCF-3 and TCF-4, directly bind to cytosolic beta-catenin and facilitate its translocation to the nucleus, where these complexes induce expression of Wnt target genes.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Wnt\/β-Catenin Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1401-t-cell-factor-4-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489391469,"sku":"1401","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"p16-cdkn2a-adenovirus-ad-cmv-p16-bhv21600015","title":"p16\/CDKN2A Adenovirus (Ad-CMV-p16)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-p16 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the p16 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e p16.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ep16\/CDKN2A is a cyclin-dependent kinase inhibitor that has shown prognostic utility in some human cancers. p16 is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene.\u003c\/p\u003e\u003cp\u003ep16\/CDKN2A generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame(ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control.\u003c\/p\u003e\u003cp\u003eThis adenovirus expresses cyclin-dependent kinase inhibitor 2A (CDKN2A) isoform p16INK4a, with the first 8 amino acid deleted from the N-terminal.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying p16\/INK4 \/ Cell Cycle.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1040-p16-cdkn2a-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489424237,"sku":"1040","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"v-raf-1-murine-leukemia-viral-oncogene-homolog-1-adenovirus-ad-raf1-bhv21600081","title":"v-raf-1 murine leukemia viral oncogene homolog 1 Adenovirus (Ad-RAF1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-RAF1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the RAF1 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e RAF1.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe Raf kinases are important intermediates in signal transduction pathways. Raf-1, the prototype member of this gene family, is a 72-76 kDa cytoplasmic protein with intrinsic serine\/threonine kinase activity, is broadly expressed in many cell types and is the cellular homolog of the viral oncogene, v-Raf. Other members of the Raf gene family include Raf-A and Raf-B. Raf-1 phosphorylates and thereby activates MEK (also designated MAP kinase kinase). Ras proteins bind Raf-1, but only when Ras is in its active GTP-binding state. This interaction results in Raf-mediated MEK activation. Two more recently described Raf-related proteins, Ksr-1 and Tak1 (TGFbeta-activated kinase), function as upstream regulators of Ras signaling pathways.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying MAPK Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1381-v-raf-1-murine-leukemia-viral-oncogene-homolog-1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489686381,"sku":"1381","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"p53-r175h-adenovirus-ad-p53-r175h-bhv21600041","title":"p53 (R175H) Adenovirus (Ad-p53-R175H)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-p53-R175H is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the R175H gene with a eGFP epitope tag under the p53 promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (p53):\u003c\/strong\u003e a p53-responsive promoter element.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e R175H (eGFP tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThis adenovirus express a common tumor-derived mutant form of p53 (R175H).\u003c\/p\u003e\u003cp\u003eReference: Yu J., et al., PNAS (1999) 96: 14517; Chan TA., et al., Genes Dev (00) 14:1584\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying p53 Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1261-p53-r175h-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489817453,"sku":"1261","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"caspase-recruitment-domain-family-member-4-adenovirus-ad-nod1-bhv21600107","title":"Caspase recruitment domain family, member 4 Adenovirus (Ad-NOD1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-NOD1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the NOD1 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e NOD1.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe mammalian homologs of the Ced-4 proteins, Apaf-1 (Ced-4), Nod1 (CARD4) and Nod2 contain a caspase recruitment domain (CARD) and a putative nucleotide binding domain, signified by a consensus Walker’s A box (P-loop) and B box (Mg2+-binding site). Nod1 contains a putative regulatory domain and multiple leucine-rich repeats. Nod1 is a member of a growing family of intracellular proteins that share structural homology to the apoptosis regulator Apaf-1. Nod2 comprises two N-terminal CARDs, a nucleotide-binding domain, and multiple C-terminal leucine-rich repeats. Mutations in Nod2 confer susceptibility to Crohn disease, a chronic inflammatory bowel disorder.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Caspase Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1408-caspase-recruitment-domain-family-member-4-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489948525,"sku":"1408","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"platelet-derived-growth-factor-beta-polypeptide-adenovirus-ad-pdgf-b-bhv21600120","title":"Platelet-derived growth factor, beta polypeptide Adenovirus (Ad-PDGF-B)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PDGF-B is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PDGF-B gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e PDGF-B.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe term ‘platelet-derived growth factor’ (PDGF) refers to a family of disulphide-bonded dimeric isoforms that are important for growth, survival and function in several types of connective tissue cells. There are four members of the platelet-derived growth factor (PDGF) family; PDGF-A, PDGF-B, PDGF-C and PDGF-D. Their biological effects are mediated via two tyrosine kinase receptors, PDGFR-alpha and PDGFR-beta, and PDGF-mediated signaling is critical for development of many organ systems.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PDGF Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1422-platelet-derived-growth-factor-beta-polypeptide-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286490014061,"sku":"1422","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"c-myc-delta-myc-adenovirus-ad-deltamyc-bhv21600047","title":"c-Myc (delta Myc) Adenovirus (Ad-deltaMyc)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-deltaMyc is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the deltaMyc gene with a eGFP epitope tag under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e deltaMyc (eGFP tag).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ec-Myc is a very strong proto-oncogene and it is very often found to be upregulated in many types of cancers. It is a mammalian transcription factor belonging to the bHLH (basic Helix Loop Helix)-Leucine Zipper family. The Myc family of cellular oncogenes, which includes c-Myc, N-Myc, L-Myc, S-Myc and B-Myc, represents nuclear transcription factors that play a significant role in cellular proliferation, differentiation, apoptosis and transformation. Members of this gene family are activated upon various mitogenic signals such as Wnt, Shh and EGF. They form heteromeric complexes with other interacting partners, such as members of the Max and Mad families, to activate transcription. Alternatively, c-Myc can also inhibit the DNA binding protein Miz-1 to repress a second set of target genes. Mnt and Mlx regulate Myc activity by forming heterodimers with Max or Mad, respectively, to suppress Myc-induced transcriptional activation.\u003c\/p\u003e\u003cp\u003eThis adenovirus contain a truncated c-Myc.\u003c\/p\u003e\u003cp\u003eReference: Hermeking H., et al., Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2229-34.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying MYC Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1286-c-myc-delta-myc-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286490276205,"sku":"1286","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"tcf-4-tcf7l2-adenovirus-ad-tcf4-bhv21600042","title":"TCF-4\/TCF7L2 Adenovirus (Ad-TCF4)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-TCF4 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the TCF4 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e TCF4.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eT cell factor-4 (Tcf-4, also known as TCF7L2) plays an important role in development and carcinogenesis. It directly binds to cytosolic β-catenin and facilitate its translocation to the nucleus. In the nucleus, these complexes induce expression various target genes.\u003c\/p\u003e\u003cp\u003eThis adenovirus contain full length human TCF4.\u003c\/p\u003e\u003cp\u003eReference: Constitutive Transcriptional Activation by a β-Catenin-Tcf Complex in APC−\/− Colon Carcinoma.  Science (275):1784-1787. 1997\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Wnt\/β-Catenin Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1280-tcf-4-tcf7l2-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286490440045,"sku":"1280","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"tumor-necrosis-factor-ligand-superfamily-member-10-adenovirus-ad-trail-bhv21600129","title":"Tumor necrosis factor (ligand) superfamily, member 10 Adenovirus (Ad-TRAIL)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-TRAIL is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the TRAIL gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e TRAIL.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eProgrammed cell death, known as apoptosis, of nonessential cells is necessary for embryogenesis, metamorphosis, tissue turnover and proper development and function of the immune system. Apoptosis causes cytoplasmic condensation, nuclear fragmentation and membrane blebbing. There are several proteins that are responsible for the balance of signals that confer cell death and\/or cell survival. Among these are the proteins of the tumor necrosis factor ligand superfamily, which includes FAS (APO-1, CD95), FAS ligand (APO-1L, CD178), TRAIL and TWEAK (APO3L) and the FAS accessory protein FAF1 (FAS-associated protein factor-1).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Death Receptors.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1431-tumor-necrosis-factor-ligand-superfamily-member-10-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286490767725,"sku":"1431","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"p27-adenovirus-ad-cmv-p27-bhv21600017","title":"p27 Adenovirus (Ad-CMV-p27)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-p27 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the p27 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e p27.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ep27 is a cyclin-dependent kinase inhibitor with many putative functions in normal and neoplastic cells. It has a role in inhibiting cell proliferation, with prognostic and therapeutic implications for human cancer.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying CDK Inhibitors.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1042-p27-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491554157,"sku":"1042","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"smad-mothers-against-dpp-homolog-5-drosophila-adenovirus-ad-smad5-bhv21600071","title":"SMAD, mothers against DPP homolog 5 (Drosophila) Adenovirus (Ad-SMAD5)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-SMAD5 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the SMAD5 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e SMAD5.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eMammalian homologs of the Drosophila Mad gene include Smad1 (also designated Madr1 or JV4-1), Smad2 (also designated Madr2 or JV18-1), Smad3, Smad4 (also designated DPC4), Smad5, Smad6, Smad7 and Smad8 (also designated Smad9). Smad1 and Smad5 are effectors of BMP2 and BMP4 function while Smad2 and Smad3 are involved in TGFb and activin-mediated growth modulation. Smad4 is required for all of the above activities and necessitates FAST-1 for DNA binding. Smad6 and Smad7 regulate the response to activin\/ TGF-beta signaling by interfering with TGF-beta-mediated phosphorylation of other Smad family members.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying TGF-β \/ WNT.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1370-smad-mothers-against-dpp-homolog-5-drosophila-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491128173,"sku":"1370","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"glycogen-synthase-kinase-3-alpha-adenovirus-ad-gsk3a-bhv21600122","title":"Glycogen synthase kinase 3 alpha Adenovirus (Ad-GSK3A)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-GSK3A is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the GSK3A gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e GSK3A.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eGlycogen synthase kinase-3 (GSK-3) is a serine\/threonine, proline directed kinase involved in a diverse array of signaling pathways, including glycogen synthesis and cellular adhesion and is implicated in Alzheimer’s disease. Two forms of GSK-3, designated GSK-3(alpha) and GSK-3(beta), are related yet they differ in their subcellular localization. The microtubule binding protein, Tau, serves to stabilize microtubules in growing axons. Tau is found to be hyperphosphorylated in paired helical filaments (PHF), the major fibrous component of neurofibrillary lesions associated with Alzheimer’s disease. Hyperphosphorylation of Tau is thought to be the critical event leading to the assembly of PHF. Six Tau protein isoforms have been identified, all of which are phosphorylated by GSK-3, presenting the possibility that miscues in GSK-3 signaling contribute to the onset of Alzheimer’s disease.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Wnt\/β-Catenin Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1424-glycogen-synthase-kinase-3-alpha-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491324781,"sku":"1424","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"tcf4-dn-adenovirus-ad-tcf4-dn-bhv21600043","title":"TCF4 (dn) Adenovirus (Ad-TCF4 (dn))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-TCF4 (dn) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the TCF4 (dn) gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e TCF4 (dn).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eT cell factor-4 (Tcf-4) plays an important role in development and carcinogenesis. It directly binds to cytosolic β-catenin and facilitate its translocation to the nucleus. In the nucleus, these complexes induce expression various target genes.\u003c\/p\u003e\u003cp\u003eThe adenovirus expresses a dominant negative TCF4.\u003c\/p\u003e\u003cp\u003eReference: He TC., et al., Science. 1998 Sep 4;281(5382):1509-12.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Wnt\/β-Catenin Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1281-tcf4-dn-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491357549,"sku":"1281","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"phosphoinositide-3-kinase-regulatory-subunit-3-p55-gamma-adenovirus-ad-pik3r3-bhv21600104","title":"phosphoinositide-3-kinase, regulatory subunit 3 (p55, gamma) Adenovirus (Ad-PIK3R3)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PIK3R3 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PIK3R3 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e PIK3R3.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ePIK3R3 is delivered to target cells via adenoviral transduction. Adenoviral delivery results in episomal (non-integrating) expression with rapid onset (typically detectable by 24 hours, peaking at 48–72 hours).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1404-phosphoinositide-3-kinase-regulatory-subunit-3-p55-gamma-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491390317,"sku":"1404","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"smad-mothers-against-dpp-homolog-2-adenovirus-ad-smad2-bhv21600086","title":"SMAD, mothers against DPP homolog 2 Adenovirus (Ad-SMAD2)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-SMAD2 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the SMAD2 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e SMAD2.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eMammalian homologs of the Drosophila Mad gene include Smad1 (also designated Madr1 or JV4-1), Smad2 (also designated Madr2 or JV18-1), Smad3, Smad4 (also designated DPC4), Smad5, Smad6, Smad7 and Smad8 (also designated Smad9). Smad1 and Smad5 are effectors of BMP2 and BMP4 function while Smad2 and Smad3 are involved in TGFb and activin-mediated growth modulation. Smad4 is required for all of the above activities and necessitates FAST-1 for DNA binding. Smad6 and Smad7 regulate the response to activin\/ TGF-beta signaling by interfering with TGF-beta-mediated phosphorylation of other Smad family members.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying TGF-β \/ WNT.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1386-smad-mothers-against-dpp-homolog-2-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491717997,"sku":"1386","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"ras-p21-protein-activator-gtpase-activating-protein-1-adenovirus-ad-rasgap-bhv21600095","title":"RAS p21 protein activator (GTPase activating protein) 1 Adenovirus (Ad-RasGAP)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-RasGAP is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the RasGAP gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e RasGAP.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eRas p21 can exist in either a physiologically quiescent GDP-binding state or a GTP-binding signal-emitting state. Interaction of Ras p21 with GTPase activating protein (GAP) can increase the rate of hydrolysis of Ras p21-bound GTP by as much as 1000-fold. In mitogenically activated and tyrosine kinase-transformed cells, Ras GAP forms a complex with a protein designated p190. At its N-terminus, p190 contains sequence motifs characteristic of all known GTPases, whereas the C-terminus contains sequences similar to those found in the Bcr gene product, n-chimerin and Rho GAP, all of which exhibit intrinsic GAP activity. Additional proteins with GTPase activating activity include GAP-associated protein p190 and Ral BP-1 (also designated RLIP 76), which displays a GAP activity specific for Rac 1 and Cdc42, Gap1m and oligophrenin-1. Oligophrenin-1 is a RhoGAP protein that stimulates GTP hydrolysis of Rho subfamily members and is involved in cell migration, morphogenesis and axon outgrowth.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying RAS\/RAF\/MEK\/ERK Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1395-ras-p21-protein-activator-gtpase-activating-protein-1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286491750765,"sku":"1395","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"b-cell-cll-lymphoma-2-adenovirus-ad-bcl2-bhv21600110","title":"B-cell CLL\/lymphoma 2 Adenovirus (Ad-BCL2)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-BCL2 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the BCL2 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e BCL2.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eMembers of the Bcl-2 family of proteins interact to regulate programmed cell death (apoptosis). Various homodimers and heterodimers formed by proteins in this family either promote or inhibit apoptosis. Pro-apoptotic members of this family include Bax, Bcl-xS, Bad, Bak, NBK (Bik), BID, Hrk, Bok, Bim, NOXA, Diva and Bmf. Apoptotic inhibitors include Bcl-2, Bcl-xL, Bcl-x(beta), Bcl-x(gamma), Bcl-w, Mcl-1, Bag-1, A1 (Bfl-1), BAR and BI-1 (TEGT). Bok, or Bcl-2 related ovarian killer, induces apoptosis in cells, but is suppressed by anti-apoptotic Bcl-2 family proteins. BECN1 plays a significant role in autophagy. PUMA gene encodes two BH3 domain-containing proteins PUMA(alpha) and PUMA(beta), which have similar binding activities to Bcl-2, localize to the mitochondria to induce cytochrome c release and activate the rapid induction of programmed cell death.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying BCL-2 Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1412-b-cell-cll-lymphoma-2-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286492078445,"sku":"1412","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"platelet-derived-growth-factor-receptor-beta-polypeptide-adenovirus-ad-pdgf-rbeta-bhv21600118","title":"Platelet-derived growth factor receptor, beta polypeptide Adenovirus (Ad-PDGF-R(beta))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PDGF-R(beta) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PDGF-R(beta) gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e PDGF-R(beta).\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe platelet derived growth factor receptor (PDGFR) family comprises PDGFR-(alpha) and PDGFR-(beta), which are structurally related and endowed with protein tyrosine kinase domains. These receptors bind the three PDGF ligand isoforms with different affinities. PDGFR-(alpha) can bind to both A and B subunits of PDGF, while PDGFR-(beta) can only bind the B subunit. Chromosomal translocation of the PDGFR-beta gene is linked with chronic myelomonocytic leukemia (CMML), a myelodysplastic syndrome, and demonstrates the oncogenic potential of the PDGF receptors.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PDGF Family.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1420-platelet-derived-growth-factor-receptor-beta-polypeptide-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286492406125,"sku":"1420","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"lymphoid-enhancer-binding-factor-1-adenovirus-ad-lef1-bhv21600154","title":"Lymphoid enhancer-binding factor 1 Adenovirus (Ad-LEF1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-LEF1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the LEF1 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e LEF1.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eT-cell factor (TCF-1) and lymphoid enhancer-binding factor (for LEF-1, also designated TCF-1(alpha)) compose a family of DNA-binding transcriptional activators that are essential for lymphoid cell development. These transcription factors are activated by the Wnt-1 and Wingless pathways and are characterized by the presence of a conserved protein motif, the high mobility group (HMG) 1 box, which mediates DNA binding. LEF-1, TCF-1, and two other family members, TCF-3 and TCF-4, directly bind to cytosolic beta-catenin and facilitate its translocation to the nucleus, where these complexes induce expression of Wnt target genes.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Wnt\/β-Catenin Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1457-lymphoid-enhancer-binding-factor-1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286492701037,"sku":"1457","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"smad-mothers-against-dpp-homolog-3-drosophila-adenovirus-ad-smad3-bhv21600157","title":"SMAD, mothers against DPP homolog 3 (Drosophila) Adenovirus (Ad-SMAD3)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-SMAD3 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the SMAD3 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e SMAD3.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eMammalian homologs of the Drosophila Mad gene include Smad1 (also designated Madr1 or JV4-1), Smad2 (also designated Madr2 or JV18-1), Smad3, Smad4 (also designated DPC4), Smad5, Smad6, Smad7 and Smad8 (also designated Smad9). Smad1 and Smad5 are effectors of BMP2 and BMP4 function while Smad2 and Smad3 are involved in TGFb and activin-mediated growth modulation. Smad4 is required for all of the above activities and necessitates FAST-1 for DNA binding. Smad6 and Smad7 regulate the response to activin\/ TGFb signaling by interfering with TGFb-mediated phosphorylation of other Smad family members.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying TGF-β \/ WNT.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1460-smad-mothers-against-dpp-homolog-3-drosophila-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286493061485,"sku":"1460","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"phosphatidylinositol-3-kinase-catalytic-delta-polypeptide-adenovirus-ad-pi3k-delta-bhv21600177","title":"phosphatidylinositol 3-kinase catalytic delta polypeptide Adenovirus (Ad-PI3K-Delta)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PI3K-Delta is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PI3K-Delta gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e PI3K-Delta.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ePI3K-Delta is delivered to target cells via adenoviral transduction. Adenoviral delivery results in episomal (non-integrating) expression with rapid onset (typically detectable by 24 hours, peaking at 48–72 hours).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying PI3K\/AKT Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1481-phosphatidylinositol-3-kinase-catalytic-delta-polypeptide-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286494077293,"sku":"1481","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"v-raf-murine-sarcoma-3611-viral-oncogene-homolog-gene-adenovirus-ad-a-raf-bhv21600205","title":"v-raf murine sarcoma 3611 viral oncogene homolog Gene Adenovirus (Ad-A-Raf)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-A-Raf is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the A-Raf gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e A-Raf.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe Raf kinases are important intermediates in signal transduction pathways. Raf-1, the prototype member of this gene family, is a 72-76 kDa cytoplasmic protein with intrinsic serine\/threonine kinase activity, is broadly expressed in many cell types and is the cellular homolog of the viral oncogene, v-Raf. Other members of the Raf gene family include Raf-A and Raf-B. Raf-1 phosphorylates and thereby activates MEK (also designated MAP kinase kinase). Ras proteins bind Raf-1, but only when Ras is in its active GTP-binding state. This interaction results in Raf-mediated MEK activation. Two more recently described Raf-related proteins, Ksr-1 and Tak1 (TGF-beta-activated kinase), function as upstream regulators of Ras signaling pathways.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying MAPK Pathway.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1510-v-raf-murine-sarcoma-3611-viral-oncogene-homolog-gene-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286494339437,"sku":"1510","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"jun-b-proto-oncogene-adenovirus-ad-jun-b-bhv21600230","title":"Jun B proto-oncogene Adenovirus (Ad-JUN B)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-JUN B is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the JUN B gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e JUN B.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThe activator protein-1 (AP-1) transcription factor consists of either Jun homodimers or Fos\/Jun heterodimeric complexes, which bind the palindromic TRE sequence TGA(C\/G)TCA. The Jun family includes c-Jun, Jun B and Jun D, while the Fos gene family members include c-Fos, Fos B, Fra-1 and Fra-2. In addition, certain ATF\/CREB proteins form leucine zipper dimers with Fos and Jun, which exhibit different specificities for AP-1 and CRE DNA motifs. AP-1 transcription factor components are subject to regulation by both phosphorylation and by chemical oxidation of specific cysteine residues mapping within the DNA binding domains of Fos and Jun. Oxidation is reversible by a cellular redox\/DNA repair protein designated Ref-1 (redox factor 1). JAB1 (Jun-activation domain-binding protein 1) potentiates transcription by either c-Jun or Jun D.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying AP-1 \/ Stress Response.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1535-jun-b-proto-oncogene-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286494994797,"sku":"1535","price":690.0,"currency_code":"USD","in_stock":true}]}],"url":"https:\/\/www.ebiohippo.com\/collections\/rtc-cancer-oncology-signaling-vectors-viruses.oembed?page=3","provider":"BioHippo","version":"1.0","type":"link"}