{"product_id":"chk2-checkpoint-homolog-s-pombe-adenovirus-ad-chk2-chek2-bhv21600223","title":"CHK2 checkpoint homolog (S. pombe) Adenovirus (Ad-CHK2\/CHEK2)","description":"\u003ch2\u003eOverview\u003c\/h2\u003e\u003cp\u003eAd-CHK2\/CHEK2 is a replication-defective recombinant human adenovirus type 5 (Ad5) expressing the CHK2\/CHEK2 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 CHK2\/CHEK2.\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\u003eDNA damage or incomplete replication of DNA results in the inhibition of cell cycle progression at the G1 to S or the G2 to M phase transition by conserved regulatory mechanisms known as cell cycle checkpoints. Checkpoint proteins include Rad17, which is involved in regulating cell cycle progression at the G1 checkpoint, and Chk1, Chk2, Rad1, Rad9 and Hus1, which are involved in regulating cell cycle arrest at the G2 checkpoint. CHEK2 is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. In addition, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Also, mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine\/threonine protein kinases.\u003c\/p\u003e\u003ch2\u003eResearch relevance and current trends\u003c\/h2\u003e\u003cul\u003e\n\u003cli\u003eDecision-relevant for researchers studying Chk2\/Chek2.\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\/1528-chk2-checkpoint-homolog-s-pombe-adenovirus\/\n--\u003e","brand":"Vector Biolabs","offers":[{"title":"1x10^10 PFU\/ml \/ 200 µL","offer_id":53286494372205,"sku":"1528","price":690.0,"currency_code":"USD","in_stock":true}],"url":"https:\/\/www.ebiohippo.com\/products\/chk2-checkpoint-homolog-s-pombe-adenovirus-ad-chk2-chek2-bhv21600223","provider":"BioHippo","version":"1.0","type":"link"}