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Background
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Checkpoint pathways control the order and timing of cell cycle transitions and ensure that critical events, such as DNA replication and chromosome segregation, are completed with high fidelity. The protein exhibits altered mobility in immunoblotting when isolated from cells treated with ionizing radiation (IR), indicating that CHK1 is modified in response to DNA damage. In vitro, CHK1 directly phosphorylates a regulator of CDC2 tyrosine phosphorylation, CDC25C. Evidence indicates that in response to DNA damage, CHK1 phosphorylates and inhibits CDC25C, thus preventing activation of the CDC2-cyclin B complex and mitotic entry. Proteolysis of activated CHK1 may promote checkpoint termination under normal conditions and may play a role in the cytotoxic effects of camptothecin and related anticancer drugs.
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Background
References
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- OConnell, M.J. Chk1 is a Wee1 kinase in the G2 DNA damage checkpoint inhibiting Cdc2 by Y15 phosphorylation. EMBO J. 1998. 16: 545-554.
- Matsuoka, S. Linkage of ATM to cell cycle regulation by the Chk2 protein kinase. Science 1998. 282: 1893-1897.
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