{"product_id":"p16-cdkn2a-adenovirus-ad-cmv-p16-bhv21600015","title":"p16\/CDKN2A Adenovirus (Ad-CMV-p16)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CMV-p16 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the p16 gene under the CMV promoter. The vector backbone has E1 and E3 deleted, rendering it non-replicative and accommodating the transgene cassette.\u003c\/p\u003e\u003ch2\u003eKey elements and design rationale\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eBackbone:\u003c\/strong\u003e Human adenovirus type 5 (Ad5) with E1 and E3 deleted (dE1\/E3). Replication-incompetent in standard cells; replication-competent helper cells (HEK293) are required for amplification.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePromoter (CMV):\u003c\/strong\u003e a strong, ubiquitous promoter active in most mammalian cell types.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTransgene:\u003c\/strong\u003e p16.\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eTiter \u0026amp; format:\u003c\/strong\u003e 1×10\u003csup\u003e10\u003c\/sup\u003e PFU\/ml in storage buffer (DMEM, 2% BSA, 2.5% glycerol or equivalent), supplied as a 200 µL aliquot.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eBiological background\u003c\/h2\u003e\u003cp\u003ep16\/CDKN2A is a cyclin-dependent kinase inhibitor that has shown prognostic utility in some human cancers. p16 is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene.\u003c\/p\u003e\u003cp\u003ep16\/CDKN2A generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame(ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control.\u003c\/p\u003e\u003cp\u003eThis adenovirus expresses cyclin-dependent kinase inhibitor 2A (CDKN2A) isoform p16INK4a, with the first 8 amino acid deleted from the N-terminal.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eUsed in oncology research to model gain-of-function or loss-of-function alterations in tumor-relevant pathways.\u003c\/li\u003e\n\u003cli\u003eAdenoviral delivery enables high-efficiency transduction of cancer cell lines and primary tumor cells.\u003c\/li\u003e\n\u003cli\u003eDecision-relevant for researchers studying p16\/INK4 \/ Cell Cycle.\u003c\/li\u003e\n\u003cli\u003eAdenovirus-mediated delivery is well-established in primary cells, organoids, and small-animal models.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eCommon research applications\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003ePathway activation studies in cell lines and primary cells.\u003c\/li\u003e\n\u003cli\u003eGain-of-function phenotyping in disease-relevant cell models.\u003c\/li\u003e\n\u003cli\u003eRescue experiments paired with shRNA knockdown of the same target.\u003c\/li\u003e\n\u003c\/ul\u003e\u003ch2\u003eNotes for experimental interpretation\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eAdenoviral delivery is episomal and non-integrating; expression dilutes with cell division and typically lasts 1–2 weeks in dividing cells (longer in non-dividing cells such as hepatocytes, neurons, and cardiomyocytes).\u003c\/li\u003e\n\u003cli\u003ePre-existing anti-Ad5 neutralizing antibodies are common in human and primate hosts and can reduce in vivo transduction; this is less relevant in inbred laboratory mouse strains.\u003c\/li\u003e\n\u003cli\u003eMOI optimization is essential — over-dosing can cause cytopathic effects; under-dosing yields incomplete transduction. A 3–5× MOI titration in your specific cell or animal model is recommended.\u003c\/li\u003e\n\u003cli\u003eReplication-defective Ad5 vectors are typically handled at BSL-2; consult your institutional biosafety officer for specific transgenes and routes of use.\u003c\/li\u003e\n\u003c\/ul\u003e\u003c!-- Sources (internal):\n  - NCBI Gene: https:\/\/www.ncbi.nlm.nih.gov\/gene\n  - UniProt: https:\/\/www.uniprot.org\/\n  - Russell WC. Adenoviruses: update on structure and function. J Gen Virol 2009; 90:1–20.\n  - Alba R, Bosch A, Chillon M. Gutless adenovirus: last-generation adenovirus for gene therapy. Gene Ther 2005; 12 Suppl 1:S18–27.\n  - Vendor reference: https:\/\/www.vectorbiolabs.com\/product\/1040-p16-cdkn2a-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286489424237,"sku":"1040","price":475.0,"currency_code":"USD","in_stock":true}],"url":"https:\/\/www.ebiohippo.com\/products\/p16-cdkn2a-adenovirus-ad-cmv-p16-bhv21600015","provider":"BioHippo","version":"1.0","type":"link"}