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Chk1 versus Cdc25: Chking One’s Levels of Cellular Proliferation

Michael H. Lam and Jeffrey M. Rosen

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This review summarizes recent studies which have provided new insight into the mechanisms by which the DNA damage response kinase, Chk1 inhibits the dual specificity phosphatase, Cdc25, and thereby regulates cell cycle progression. Recently, Chk1 has been shown to not only regulate Cdc25A degradation but also its ability to interact with various Cdk complexes through phosphorylation of the carboxy-terminus of the phosphatase. Surprisingly, these effects appear to be specific for Chk1, but not Chk2, which may explain the recently reported in vivo haploinsufficiency phenotype observed in the mammary gland using a Chk1 conditional mouse model.

Authors

Michael H. Lam

Jeffrey M. Rosen

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If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.