Chk2 / Unconjugated /

Product Details
Description The p53 tumor-suppressor gene integrates numerous signals that control cell life and death. Several novel molecules involved in p53 signaling, including Chk2 , p53R2 (2), p53AIP1 (3), Noxa (4), PIDD (5), and PID/MTA2 (6), were recently discovered. The checkpoint kinase Chk2 is the mammalian homologue of yeast Cds1/Rad53. In response to DNA damage, the checkpoint kinase ATM phosphorylates and activates Chk2, which in turn directly phosphorylates and activates p53 (7,8). Chk2 serves as ATM downstream effector to mediate activation of p53. Chk2 also phosphorylates and activates BRCA1, the product of a tumor suppressor gene that is mutated in breast and ovarian cancer (9).
Conjugate Unconjugated
Clone
Target Species Human
Applications ELISA, WB
Supplier Leinco
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About Chk2
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]
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