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CHEK2 Matched Antibody Pair (268) (APMAB-268LY)


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Specifications

ApplIcation
Sandwich ELISA
Specificity
Human
Capture Antibody
Rabbit anti-CHEK2 polyclonal antibody, 100 ug
Detection Antibody
Anti-CHEK2 Mouse monoclonal, IgG2a antibody, 20 ug
Dilutions
10 ng/ml-100 ng/ml
Format
Liquid
Storage
Aliquot and store at -20°Cor -80°C. Avoid freeze-thaw cycles.
Introduction
In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by this gene 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. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2012]
Alternative Names
Checkpoint Kinase 2; CHK2 Checkpoint Homolog; Cds1 Homolog; HuCds1; RAD53; HCds1; CDS1; CHK2; Serine/Threonine-Protein Kinase Chk2;
Entrez Gene ID
11200
UniProt ID
O96017
More Infomation

Mustofa, M. K., Tanoue, Y., Tateishi, C., Vaziri, C., & Tateishi, S. (2020). Roles of Chk2/CHEK2 in guarding against environmentally induced DNA damage and replication‐stress. Environmental and Molecular Mutagenesis, 61(7), 730-735.

Mandelker, D., Kumar, R., Pei, X., Selenica, P., Setton, J., Arunachalam, S., ... & Reis-Filho, J. S. (2019). The landscape of somatic genetic alterations in breast cancers from CHEK2 germline mutation carriers. JNCI cancer spectrum, 3(2), pkz027.

AlDubayan, S. H., Pyle, L. C., Gamulin, M., Kulis, T., Moore, N. D., Taylor-Weiner, A., ... & Lessel, D. (2019). Association of inherited pathogenic variants in checkpoint kinase 2 (CHEK2) with susceptibility to testicular germ cell tumors. JAMA oncology, 5(4), 514-522.

Ansari, N., Shahrabi, S., Khosravi, A., Shirzad, R., & Rezaeean, H. (2019). Prognostic significance of CHEK2 mutation in progression of breast cancer. Laboratory medicine, 50(3), e36-e41.

Luo, L., Gao, W., Wang, J., Wang, D., Peng, X., Jia, Z., ... & Wang, Y. (2018). Study on the mechanism of cell cycle checkpoint kinase 2 (CHEK2) gene dysfunction in chemotherapeutic drug resistance of triple negative breast cancer cells. Medical science monitor: international medical journal of experimental and clinical research, 24, 3176.

Huszno, J., & Kołosza, Z. (2018). Checkpoint kinase 2 (CHEK2) mutation in renal cell carcinoma: a single-center experience. Journal of Kidney Cancer and VHL, 5(1), 19.

Liang, M., Zhang, Y., Sun, C., Rizeq, F. K., Min, M., Shi, T., & Sun, Y. (2018). Association between CHEK2* 1100delC and breast cancer: a systematic review and meta-analysis. Molecular diagnosis & therapy, 22(4), 397-407.

Aldubayan, S. H., Pyle, L. T., Loud, J. T., Greene, M. H., Sweeney, C., Nathanson, K., ... & Lessel, D. (2018). Inherited defects in checkpoint kinase 2 (CHEK2) to confer increased susceptibility to testicular germ cell tumors.

Apostolou, P., & Papasotiriou, I. (2017). Current perspectives on CHEK2 mutations in breast cancer. Breast Cancer: Targets and Therapy, 9, 331.

Hong, Y., Shi, J., Ge, Z., & Wu, H. (2017). Associations between mutations of the cell cycle checkpoint kinase 2 gene and gastric carcinogenesis. Molecular medicine reports, 16(4), 4287-4292.

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For research use only. Not intended for any clinical use.

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