{"title":"Adenoviral Vectors","description":"","products":[{"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":"foxo3a-adenovirus-ad-gfp-foxo3a-bhv21600008","title":"FOXO3A Adenovirus (Ad-GFP-FOXO3A)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-GFP-FOXO3A is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the GFP-FOXO3A 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 GFP-FOXO3A (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 contains both a wild type FOXO3A gene and a GFP as a marker. The Foxo3a has a HA tag.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Gfp-Foxo3A.\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\/1026-foxo3a-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487753069,"sku":"1026","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"nod2-card15-adenovirus-ad-cmv-nod2-bhv21600028","title":"Nod2 (CARD15) Adenovirus (Ad-CMV-Nod2)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Nod2 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Nod2 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 Nod2.\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\u003eNucleotide-binding oligomerization domain protein 2 The mammalian homologs of the Ced-4 proteins, Apaf-1 (Ced-4), Nod1 (CARD4), and Nod2 (CARD15) 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). Nod2 is composed of two N-terminal CARDs, a nucleotide-binding domain, and multiple C-terminal leucine-rich repeats. The expression of Nod2 is highly restricted to monocytes, and activates NFκB in response to bacterial lipopolysaccharides.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Pattern Recognition.\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\/1141-nod2-card15-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487785837,"sku":"1141","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"cre-recombinase-adenovirus-ad-cmv-icre-bhv21600020","title":"Cre Recombinase Adenovirus (Ad-CMV-iCre)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-iCre is a replication-defective recombinant Ad5 adenovirus expressing the iCre recombinase under the CMV promoter. It is used to deliver Cre activity to floxed alleles in cell lines and in vivo for conditional gene knockout, lineage tracing, and activation of Cre-dependent (DIO\/FLEX) reporters.\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 iCre.\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 Cre recombinant adenovirus expresses Cre recombinase, a Type I topoisomerase from P1 bacteriophage that catalyzes site-specific recombination of DNA between loxP sites. loxP is a 34 bp DNA sequence at which confers directionality. Cre recombinase is used as a tool to genetically modify genes, such as to delete a segment of DNA flanked by LoxP sites in cultured cells or experimental animals.\u003c\/p\u003e\u003cp\u003eThis adenovirus expresses a codon improved Cre (iCre) under a CMV promoter.\u003c\/p\u003e\u003cp\u003eCheck out this instruction video on using our adenovirus Cre to knockout LoxP flanked gene in primary mouse embryonic fibroblasts (MEF).\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Recombinases.\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\u003eConditional gene knockout in floxed-allele cell lines and animals.\u003c\/li\u003e\n\u003cli\u003eLineage tracing using Cre-dependent reporter alleles.\u003c\/li\u003e\n\u003cli\u003eActivation of Cre-dependent (DIO\/FLEX) viral reporters or effectors.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eRecombination efficiency depends on Cre expression level, allele accessibility, and the time window assayed; allow 72–96 hours after infection for recombination to plateau.\u003c\/li\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  - Sauer B, Henderson N. Site-specific DNA recombination in mammalian cells by the Cre recombinase of bacteriophage P1. Proc Natl Acad Sci USA 1988; 85:5166–70.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1045-cre-recombinase-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487818605,"sku":"1045","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":"tlr2-adenovirus-ad-cmv-tlr2-bhv21600029","title":"TLR2 Adenovirus (Ad-CMV-TLR2)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-TLR2 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the TLR2 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 TLR2.\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\u003eToll-like Receptor 2 Six human homologs of the Drosophila Toll receptor were initially identified based on their sequence similarities and designated tolllike receptors (TLR). Toll receptors are involved in mediating dorsoventral polarization in the developing Drosophila embryo and also participate in the host immunity. The TLR family of proteins are characterized by a highly conserved Toll homology (TH) domain, which is essential for Toll-induced signal transduction. TLR1, as well as the other TLR family members, are type I transmembrane receptors that characteristically contain an extracellular domain consisting of several leucine-rich regions along with a single cytoplasmic Toll\/IL-1R-like domain. TLR2 and TLR4 are activated in response to lipopolysacchride (LPS) stimulation, which results in the activation and translocation of NFκB and suggests that these receptors are involved in mediating inflammatory responses. Expression of TLR receptors is highest in peripheral blood leukocytes, macrophages, and monocytes.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Pattern Recognition.\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\/1142-tlr2-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286487884141,"sku":"1142","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":"human-hsp70-adenovirus-ad-cmv-hsp70-bhv21600022","title":"human HSP70 Adenovirus (Ad-CMV-HSP70)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-HSP70 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the HSP70 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 HSP70.\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\u003eHeat shock protein Hsp70\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Hsp70.\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\/1047-human-hsp70-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488015213,"sku":"1047","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"egfp-adenovirus-ad-gfp-bhv21600023","title":"eGFP Adenovirus (Ad-GFP)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-GFP is a replication-defective recombinant Ad5 adenovirus expressing the GFP reporter gene under the CMV 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 (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 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\u003eThis recombinant human adenovirus type 5 expresses enhanced green fluorescent protein under the control of a CMV promoter. Green fluorescent protein (GFP) is a protein originally isolated from the jellyfish that fluoresces green when exposed to blue light. Enhanced GFP (eGFP) is a GFP mutant with improved fluorescence and stability. Recombinant eGFP adenovirus serves as a control for other recombinant adenoviruses. Since GFP is easily visualized under fluorescence microscopy, this adenovirus can also be used to determine the transduction efficiency and to optimize viral infection condition in a specific cell type.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Reporter Vectors.\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\/1060-egfp-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488047981,"sku":"1060","price":395.0,"currency_code":"USD","in_stock":true}]},{"product_id":"gata6-adenovirus-ad-cmv-gata6-bhv21600009","title":"GATA6 Adenovirus (Ad-CMV-GATA6)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-GATA6 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the GATA6 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 GATA6 (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\u003eTranscription factor GATA6\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Lineage TFs.\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\/1027-gata6-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488080749,"sku":"1027","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":"catenin-beta-adenovirus-ad-cmv-catenin-beta-bhv21600036","title":"catenin (beta) Adenovirus (Ad-CMV-catenin (beta))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-catenin (beta) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the catenin (beta) 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 catenin (beta) (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 catenins, α , β and γ , are proteins which bind to the highly conserved, intracellular cytoplasmic tail of E-cadherin. Together, the catenin\/cadherin complexes play an important role mediating cellular adhesion. α-catenin, a 102 kDa protein, was initially described as an E-cadherin associated protein, and since has been shown to associate with other members of the cadherin family, such as N-cadherin and P-cadherin. The 92 kDa β-catenin associates with the cytoplasmic portion of E-cadherin, which is necessary for the func-tion of E-cadherin as an adhesion molecule. β-catenin has also been found in complexes with the tumor suppressor protein APC. γ-catenin, also known as plakoglobin, is an 82 kDa protein that binds with α-catenin and N-cad-herin.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Catenin.\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\/1182-catenin-beta-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488113517,"sku":"1182","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":"ikba-s32a-s36a-adenovirus-ad-cmv-ikbdn-bhv21600010","title":"iKBa (S32A\/S36A) Adenovirus (Ad-CMV-iKB(DN))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-iKB(DN) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the iKB(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 iKB(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 the dominant-negative mutant of I kappa B alpha (IkBa-S32A\/S36A), which has serine-to-alanine substitutions at amino acids 32 and 36, respectively, and is resistant to phosphorylation-induced degradation of I kappa B alpha.\u003c\/p\u003e\u003cp\u003eReferences: Kumar, A., Eby, M. T., Sinha, S., Jasmin, A., and Chaudhary, P. M. (2000) J. Biol. Chem. 276, 2668-2677\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying NF-κB 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\/1028-ikba-s32a-s36a-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488179053,"sku":"1028","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":"foxo3a-aaa-adenovirus-ad-cmv-fkhrl1-aaa-bhv21600007","title":"FOXO3A (AAA) Adenovirus (Ad-CMV-FKHRL1 (AAA))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-FKHRL1 (AAA) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the FKHRL1 (AAA) gene with a HA\/GFP 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 FKHRL1 (AAA) (HA\/GFP 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 FKHRL1-AAA triple mutant is not phosphorylatable because three phosphorylation sites, Thr32, Ser253, and Ser315, were replaced by alanine residues.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Fkhrl1.\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\/1025-foxo3a-aaa-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488244589,"sku":"1025","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":"luciferase-rnai-adenovirus-ad-u6-luc-rnai-bhv21600026","title":"Luciferase RNAi Adenovirus (Ad-U6-Luc-RNAi)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-U6-Luc-RNAi is a replication-defective recombinant Ad5 adenovirus driving short hairpin RNA (shRNA) expression — an shRNA cassette targeting Luc — under a U6 Pol III promoter for stable, efficient knockdown. Adenoviral delivery enables shRNA-mediated silencing in difficult-to-transfect cell types and in vivo tissues where transient transfection is inefficient.\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 (U6):\u003c\/strong\u003e a Pol III promoter that drives short non-coding RNA (shRNA\/sgRNA) expression.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e Luc-RNAi (fLuc 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\u003cli\u003e\n\u003cstrong\u003eshRNA cassette:\u003c\/strong\u003e Pol III-driven hairpin expression for stable knockdown; the transcribed shRNA is processed into a functional siRNA by Dicer and loaded into RISC for sequence-specific mRNA cleavage or translational repression.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eRNAi adenovirus targeting the Luciferase. Generally used as a RNAi control adenovirus.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying RNAi Controls.\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\u003eLoss-of-function knockdown in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003ePathway interrogation paired with matched scrambled-shRNA controls.\u003c\/li\u003e\n\u003cli\u003eIn vivo knockdown via tissue-targeted intravenous or local delivery.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eConfirm target depletion at the protein level (Western blot) in addition to mRNA-level (qPCR), and verify with a non-targeting scrambled-shRNA control.\u003c\/li\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  - Brummelkamp TR et al. A system for stable expression of short interfering RNAs in mammalian cells. Science 2002; 296:550–3.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1123-luciferase-rnai-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488342893,"sku":"1123","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"luciferase-adenovirus-ad-cmv-luc-bhv21600001","title":"Luciferase Adenovirus (Ad-CMV-Luc)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Luc is a replication-defective recombinant Ad5 adenovirus expressing the Luc reporter gene under the CMV 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 (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 Luc (fLuc 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\u003eLuciferase is a class of oxidative enzymes used in bioluminescence and is distinct from a photoprotein. In the luciferase reaction, light is emitted when luciferase acts on the appropriate luciferin substrate. Photon emission can be detected by light sensitive apparatus such as a luminometer or modified optical microscopes. luciferase commonly is used as a reporter to assess the transcriptional activity in cells.\u003c\/p\u003e\u003cp\u003eThis adenovirus expresses Luciferase under the control of CMV promoter.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Reporter Vectors.\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\/1000-luciferase-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488375661,"sku":"1000","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"retinoblastoma-like-2-p130-adenovirus-ad-p130-bhv21600096","title":"Retinoblastoma-like 2 (p130) Adenovirus (Ad-p130)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-p130 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the p130 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 p130.\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\u003eDecision-relevant for researchers studying P130.\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\/1396-retinoblastoma-like-2-p130-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488408429,"sku":"1396","price":690.0,"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":"src-adenovirus-ad-cmv-src-bhv21600032","title":"Src Adenovirus (Ad-CMV-Src)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-Src is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the Src 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 Src.\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\u003eSeveral protein tyrosine kinases (Src, Fyn, Lyn, Yes, Lck, Hck, etc) have been identified within the Src gene family. On the basis of their associations with specific cell surface receptors, Src gene family members play critical roles in various signal transduction pathways.\u003c\/p\u003e\u003cp\u003eSrc is regulated by tyrosine phosphorylation at two sites with opposite effects. Phosphorylation of Tyr 416 in the activation loop of the kinase domain upregulates the enzyme; Phosphorylation of Tyr 527 in the C-terminal by CSK inhibits the enzyme activity.\u003c\/p\u003e\u003cp\u003eThis adenovirus has a Src activating and signaling molecule.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Src.\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\/1166-src-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488473965,"sku":"1166","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":"ikk-alpha-ikka-adenovirus-ad-cmv-ikka-bhv21600035","title":"IKK-alpha (IKKa) Adenovirus (Ad-CMV-IKKa)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-IKKa is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the IKKa 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 IKKa.\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\u003eIKKα The transcription factor NFκB is retained in the cytoplasm in an inactive form by the inhibitory protein IκB. Activation of NFκB requires that IκB be phosphorylated on specific serines residues, which results in targeted degradation of IκB. IκB kinase α (IKKα), previously designated CHUK, interacts with IκB-α and specifically phosphorylates IκB-α on the sites that trigger its degradation, serines 32 and 36. IKKα appears to be critical for NFκB activation in response to proinflammatory cytokines. Phosphorylation of IκB by IKKα is stimulated by the NFκB inducing kinase (NIK), which itself is a central regulator for NFκB activation in response to TNF and IL-1. The functional IKK complex contains three subunits, IKKα , IKKβ and IKKγ (also designated NEMO), and each appear to make essential contributions to IκB phosphorylation.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying NF-κB 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\/1181-ikk-alpha-ikka-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488637805,"sku":"1181","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"scrambled-shrna-with-gfp-adenovirus-ad-gfp-u6-shrna-bhv21600025","title":"Scrambled shRNA with GFP Adenovirus (Ad-GFP-U6-shRNA)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-GFP-U6-shRNA is a replication-defective recombinant Ad5 adenovirus driving short hairpin RNA (shRNA) expression — an shRNA cassette targeting GFP-U6 — under a CMV + U6 Pol III promoter for stable, efficient knockdown. Adenoviral delivery enables shRNA-mediated silencing in difficult-to-transfect cell types and in vivo tissues where transient transfection is inefficient.\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 + U6):\u003c\/strong\u003e the promoter governs cell-type and strength of expression.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e GFP-U6-shRNA (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\u003cli\u003e\n\u003cstrong\u003eshRNA cassette:\u003c\/strong\u003e Pol III-driven hairpin expression for stable knockdown; the transcribed shRNA is processed into a functional siRNA by Dicer and loaded into RISC for sequence-specific mRNA cleavage or translational repression.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003eThis adenovirus contains a scramble shRNA sequence under the control of U6 promoter, with the GFP co-expression under a CMV promoter.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Gfp-U6 (RNAi).\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\u003eLoss-of-function knockdown in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003ePathway interrogation paired with matched scrambled-shRNA controls.\u003c\/li\u003e\n\u003cli\u003eIn vivo knockdown via tissue-targeted intravenous or local delivery.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eConfirm target depletion at the protein level (Western blot) in addition to mRNA-level (qPCR), and verify with a non-targeting scrambled-shRNA control.\u003c\/li\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  - Brummelkamp TR et al. A system for stable expression of short interfering RNAs in mammalian cells. Science 2002; 296:550–3.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1122-scrambled-shrna-with-gfp-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488670573,"sku":"1122","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"nk2-transcription-factor-related-locus-5-drosophila-adenovirus-ad-nkx2-5-csx-bhv21600115","title":"NK2 transcription factor related, locus 5 (Drosophila) Adenovirus (Ad-NKX2.5\/CSX)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-NKX2.5\/CSX is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the NKX2.5\/CSX 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 NKX2.5\/CSX.\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 Nkx family of homeobox containing transcription factors are differentially expressed and regulate the production of tissue specific target genes. Some members of the Nkx family include TTF-1 (also designated Nkx-2.1), Nkx-2.2, Nkx-2.5 (also designated cardiac specific homeobox protein CSX), Nkx-2.6, Nkx-3.1, Nkx-3.2, Nkx-6.1 and Nkx-6.2. TTF-1 is primarily observed in adult thyroid and lung. Nkx-2.2 and Nkx-6.1 are required for pancreatic B-cell differentiation, and Nkx-2.5 and Nkx-2.6 are involved in normal cardiac development. Nkx-3.1 is predominantly expressed in developing and adult prostate tissue.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying NF-κB 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\/1417-nk2-transcription-factor-related-locus-5-drosophila-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488703341,"sku":"1417","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"14-3-3-sigma-adenovirus-ad-sigma-bhv21600051","title":"14-3-3 sigma Adenovirus (Ad-sigma)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-sigma is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the sigma 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 sigma (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\u003e14-3-3sigma is a member of the multifunctional 14-3-3 protein family that includes beta, epsilon, gamma, eta, tau, and zeta. They recognize consensus motifs containing Arg-Ser-X-phosphoSer-X-Pro or its derivatives, and are able to bind proteins with phosphorylated serine or threonine.  Through interactions with other proteins, 14-3-3 proteins is involved in controlling a wide range of regulatory processes, such as mitogenic signal transduction, apoptotic cell death, and cell cycle control. They can function as allosteric cofactors to alter the catalytic activity or conformational state of target proteins, such as PKC, ExoS ADP-ribosyltransferase, and tyrosine and tryptophan hydroxylases. They may also act as steric regulators to prevent their protein ligands from interacting with other cellular components, hence, influence intracellular localization or complex formation. Dimeric 14-3-3 can bind two target proteins simultaneously to operate as a scaffold protein to induce protein-protein interactions. 14-3-3sigma functions as a p53-regulated inhibitor of G2\/M progression and plays a key role in maintaining G2-arrest upon DNA damage in certain cancer cells, such as the colorectal cells. They are primarily found in the cytoplasm and may be required to sequester mitotic activators cyclin B1 and cdc2 in cytoplasm. Overexpression of 14-3-3sigma can induce G2 arrest and deletion of 14-3-3sigma can lead to mitotic catastrophe upon DNA damage.\u003c\/p\u003e\u003cp\u003eThis adenovirus contain Ad-σ.\u003c\/p\u003e\u003cp\u003eReference: Hermeking H., et al., Mol Cell. 1997 Dec;1(1):3-11.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Sigma.\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\/1290-14-3-3-sigma-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488736109,"sku":"1290","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"wilms-tumor-1-adenovirus-ad-wt1-bhv21600098","title":"Wilms tumor 1 Adenovirus (Ad-WT1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-WT1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the WT1 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 WT1.\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 gene encodes a transcription factor that contains four zinc-finger motifs at the C-terminus and a proline\/glutamine-rich DNA-binding domain at the N-terminus. It has an essential role in the normal development of the urogenital system, and it is mutated in a small subset of patients with Wilm’s tumors.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Wt1.\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\/1398-wilms-tumor-1-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488768877,"sku":"1398","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"interleukin-1-alpha-adenovirus-ad-il1alpha-bhv21600068","title":"Interleukin 1, alpha Adenovirus (Ad-IL1(alpha))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-IL1(alpha) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the IL1(alpha) 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 IL1(alpha).\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 interleukins are a broad family of well characterized cytokines, primarily of hematopoietic cell origin. As new cytokines are molecularly characterized, they are assigned an IL number to maintain a standard nomenclature. The interleukins are secreted by immune cells (mainly macrophages, B-cells or T-cells) that regulate a wide range of immune system functions. The functions of different interleukins vary from regulation inflammatory and immune responses, functioning as autocrine factor and regulation and\/or inhibition of other interleukins.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Interleukins \/ TNF.\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\/1366-interleukin-1-alpha-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488801645,"sku":"1366","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"nik-adenovirus-ad-cmv-nik-bhv21600034","title":"NIK Adenovirus (Ad-CMV-NIK)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-NIK is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the NIK 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 NIK.\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\u003eNFκB-Inducing Kinase (NIK) The NFκB transcription factor can be activated by several cytokines including TNF and IL-1. The TNF receptor activates NFκB through the Traf2 adapter protein , whereas the IL-1 receptor activates NFκB in a pathway involving Traf6 . Both Traf2 and Traf6 have been shown to interact with a serine\/threonine kinase designated NFkB inducing kinase (NIK), which appears to participate in the NFκB signaling cascades triggered by both TNF and IL-1. NIK associates with, and is a costimulator for IkB kinase α (IKKα). IKKα , in turn, phosphorylates IκB, resulting in I κ B degradation and NF κ B activation. NIK has sequence similarity to several kinases that participate in MAP kinase cascades.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Nik.\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\/1180-nik-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488834413,"sku":"1180","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"mitogen-activated-protein-kinase-kinase-kinase-kinase-5-adenovirus-ad-mapkkkk5-bhv21600099","title":"Mitogen-activated protein kinase kinase kinase kinase 5 Adenovirus (Ad-MAPKKKK5)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-MAPKKKK5 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the MAPKKKK5 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 MAPKKKK5.\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 gene encodes a member of the serine\/threonine protein kinase family, that is highly similar to yeast SPS1\/STE20 kinase. Yeast SPS1\/STE20 functions near the beginning of the MAP kinase signal cascades that is essential for yeast pheromone response. This kinase was shown to activate Jun kinase in mammalian cells, which suggested a role in stress response. Two alternatively spliced transcript variants encoding the same protein have been described for this gene.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Mapkkkk5.\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\/1399-mitogen-activated-protein-kinase-kinase-kinase-kinase-5-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286488867181,"sku":"1399","price":690.0,"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":"leptin-obesity-homolog-mouse-adenovirus-ad-leptin-bhv21600139","title":"Leptin (obesity homolog, mouse) Adenovirus (Ad-LEPTIN)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-LEPTIN is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the LEPTIN 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 LEPTIN.\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 gene is similar to the mouse obesity gene (ob). The protein encoded by this gene is secreted by white adipocytes. In the mouse study, mutations in this gene are linked to severe and morbid obesity. The recessive obesity mutation, Ob, identified in 1950, results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. It has been postulated that the Ob gene product may represent a component of a signaling pathway in adipose tissue that functions to regulate body fat depot size. Ob encodes a 4.5 kb adipose tissue-specific mRNA with a highly conserved 167 amino acid open reading frame. The Ob gene product has been identified as a 16 kDa secreted protein, designated leptin, that is apparently produced only in adipose tissue.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in metabolic and endocrine research to model perturbations in lipid, glucose, or hormone signaling.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Insulin \/ Adipokines.\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\/1441-leptin-obesity-homolog-mouse-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489031021,"sku":"1441","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"b-gal-lacz-adenovirus-ad-cmv-b-gal-bhv21600024","title":"b-gal\/LacZ Adenovirus (Ad-CMV-b-Gal)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-b-Gal is a replication-defective recombinant Ad5 adenovirus expressing the b-Gal reporter gene under the CMV 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 (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 b-Gal (LacZ 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\u003ebeta-galactosidase \/ LacZ recombinant adenovirus\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Reporter Vectors.\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\/1080-b-gal-lacz-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489063789,"sku":"1080","price":395.0,"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":"rap-guanine-nucleotide-exchange-factor-gef-3-adenovirus-ad-epac1-bhv21600087","title":"Rap guanine nucleotide exchange factor (GEF) 3 Adenovirus (Ad-EPAC1)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-EPAC1 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the EPAC1 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 EPAC1.\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\u003eEpac (exchange protein directly activated by cAMP; also designated cAMP-GEFI) and Epac2 (also designated cAMP-GEFII) compose a novel family of cyclic AMP activated guanine-nucleotide exchange factors (GEFs). Both Epac and Epac2 contain cAMP-binding motifs and a motif common to Ras superfamily GEFs. Epac and Epac2 both function to activate Rap1, a Ras-like GTPase that is known to suppress the oncogenic transformation of cells by Ras. Epac is ubiquitously expressed, whereas Epac2 is primarily expressed in the brain and adrenal glands.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Epac1.\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\/1387-rap-guanine-nucleotide-exchange-factor-gef-3-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489129325,"sku":"1387","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"mek1-dn-adenovirus-ad-cmv-mek1dn-bhv21600031","title":"MEK1 (dn) Adenovirus (Ad-CMV-MEK1(dn))","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-MEK1(dn) is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the MEK1(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 MEK1(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\u003eMitogen-activated protein kinases (MAPK), including ERK1\/2, p38, and JNK1\/2, are important regulators of cell function. The ERK MAPKs are most frequently activated by mitogenes, whereas the JNK and p38 MAPKs are strongly responsive to stress and inflammatory signals. The MAPKs are activated through multiple intracellular phosphorylation cascade events. The core unit includes MAPKKKs and MAPKKs. MEK1 and MEK2 are dual-specificity proteins kinases. MEKs activates ERK1 and ERK2 by phosphorylating both threonine and tyrosine residues at sites located within the activation loop of kinase subdomain VIII.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Mek1.\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\/1165-mek1-dn-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489162093,"sku":"1165","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":"period-homolog-3-drosophila-adenovirus-ad-per3-bhv21600097","title":"Period homolog 3 (Drosophila) Adenovirus (Ad-PER3)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PER3 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PER3 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 PER3.\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 Per-Arnt-Sim (PAS) domain was identified as a 270 amino acid motif that mediates associations among various PAS family transcription factors. PAS domain family members include period proteins (Per1, Per2 and Per3), Arnt 1 (also designated HIF-1?), Arnt 2, Ah Receptor, BMAL1 (for Brain and Muscle Arnt-like protein 1; also designated Arnt 3, TIC, JAP3 or MOP3), Clock, single-minded proteins (SIM1 and SIM2) and hypoxia-inducible factors such as HIF-1a (also designated MOP1), EPAS-1 (also designated HIF-2a, MOP2 or HLF) and HIF-3a. The PAS family also contains a neuronal specific transcription factor known as NPAS2 that is involved the development and maintenance of learning and memory pathways. NPAS2, which is also designated PAS 4\/MOP4, associates with MOP3 to activate transcription.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Per3.\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\/1397-period-homolog-3-drosophila-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489227629,"sku":"1397","price":690.0,"currency_code":"USD","in_stock":true}]},{"product_id":"interleukin-6-adenovirus-ad-il6-bhv21600080","title":"Interleukin 6  Adenovirus (Ad-IL6)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-IL6 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the IL6 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 IL6.\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 interleukins are a broad family of well characterized cytokines, primarily of hematopoietic cell origin. As new cytokines are molecularly characterized, they are assigned an IL number to maintain a standard nomenclature. The interleukins are secreted by immune cells (mainly macrophages, B-cells or T-cells) that regulate a wide range of immune system functions. The functions of different interleukins vary from regulation inflammatory and immune responses, functioning as autocrine factor and regulation and\/or inhibition of other interleukins.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in immunology research to manipulate cytokine signaling, pattern recognition, or transcription factor pathways.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying Interleukins \/ TNF.\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\/1380-interleukin-6-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489260397,"sku":"1380","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"puma-adenovirus-ad-puma-bhv21600049","title":"PUMA Adenovirus (Ad-PUMA)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-PUMA is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the PUMA 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 PUMA (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\u003ePUMA (p53 up-regulated modulator of apoptosis) is a BH3-only protein.\u003c\/p\u003e\u003cp\u003eEach of the “BH3-only” group of proteins contains an amphipathic Bcl-2 homology (BH) domain. These proteins act as sensors of discrete apoptotic stimuli, antagonizing or activating the function of multidomain Bcl-2 family proteins by interacting with them. This in turn triggers a cascade of downstream events, such as the collapse of mitochondrial membrane potential, release of the apoptogenic mitochondrial proteins cytochrome c and SMAC, and activation of caspases.\u003c\/p\u003e\u003cp\u003ePUMA plays a vital role in mediating the apoptotic responses to p53. It can be activated by p53 directly through p53-responsive elements in its promoter region. The PUMA protein interacts with Bcl-XL and promotes mitochondrial translocation and multimerization of Bax.\u003c\/p\u003e\u003cp\u003eThis adenovirus expresses human PUMA fused to a HA tag.\u003c\/p\u003e\u003cp\u003eReference: Yu J., et al., Proc Natl Acad Sci U S A. 2003 Feb 18;100(4):1931-6.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Puma.\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\/1288-puma-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489293165,"sku":"1288","price":475.0,"currency_code":"USD","in_stock":true}]},{"product_id":"heat-shock-90kda-protein-1-alpha-adenovirus-ad-hsp90-bhv21600113","title":"Heat shock 90kDa protein 1, alpha Adenovirus (Ad-HSP90)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-HSP90 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the HSP90 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 HSP90.\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 heat shock proteins (HSPs) comprise a group of highly conserved, abundantly expressed proteins with diverse functions, including the assembly and sequestering of multiprotein complexes, transportation of nascent polypeptide chains across cellular membranes and regulation of protein folding. Also called molecular chaperones, heat shock proteins fall into six general families: HSP 90, HSP 70, HSP 60, the small molecular weight HSPs, the immunophilins and the HSP 110 family. The HSP 90 family consists of HSP 90(alpha), HSP 90(beta) and GRP 94, also called endoplasmin. The HSP 70 family includes HSP 70, HSC 70, GRP 78 and GRP 75. The low molecular weight family consists of HSP 10, HSP 27 (Heme Oxygenase 1), HSP 32 and HSP 40. The immunophilins include HSP 56 and bind immunosuppressant drugs. The HSP 110 family includes HSP 110, Apg-1 (also referred to as OSP 94), Apg-2 and HSP 105. HSP 47 binds specifically to collagen. Although the HSPs have long been known to bind ATP, the functional significance has not been established. Members of the HSP 70 family are implicated in acting as force generating motors, relying on the hydrolysis of ATP for their activity.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Hsp90.\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\/1415-heat-shock-90kda-protein-1-alpha-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489325933,"sku":"1415","price":690.0,"currency_code":"USD","in_stock":true}]}],"url":"https:\/\/www.ebiohippo.com\/collections\/adenoviral-vectors.oembed","provider":"BioHippo","version":"1.0","type":"link"}