This antibody is purified through a protein A column, followed by peptide affinity purification.
Immunogène
This CHEK2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 111-141 amino acids from the N-terminal region of human CHEK2.
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
4 °C,-20 °C
Date de péremption
6 months
Xiao, Zheng, Huang, Liu, Zhang, Ma: "Deficiency of 53BP1 inhibits the radiosensitivity of colorectal cancer." dans: International journal of oncology, Vol. 49, Issue 4, pp. 1600-8, (2017) (PubMed).
Yao, Huang, Zheng, Liu, Lin, Zhang, Yang, Zhang, Ma: "53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway." dans: Journal of cancer research and clinical oncology, Vol. 143, Issue 3, pp. 419-431, (2017) (PubMed).
Yang, Wood, Hrushesky: "Mammalian TIMELESS is required for ATM-dependent CHK2 activation and G2/M checkpoint control." dans: The Journal of biological chemistry, Vol. 285, Issue 5, pp. 3030-4, (2010) (PubMed).
Varmark, Kwak, Theurkauf: "A role for Chk2 in DNA damage induced mitotic delays in human colorectal cancer cells." dans: Cell cycle (Georgetown, Tex.), Vol. 9, Issue 2, pp. 312-20, (2010) (PubMed).
Zhu, Miao, Huang, Feng, Zhang, Lu, Cai, Tong, Xu, Qian, Ding: "Naphthalimides induce G(2) arrest through the ATM-activated Chk2-executed pathway in HCT116 cells." dans: Neoplasia (New York, N.Y.), Vol. 11, Issue 11, pp. 1226-34, (2009) (PubMed).
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.