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Chk1 versus Cdc25: chking one's levels of cellular proliferation.

机译:Chk1与Cdc25:抑制人的细胞增殖水平。

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摘要

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.
机译:这篇综述总结了最近的研究,这些研究为DNA损伤反应激酶Chk1抑制双重特异性磷酸酶Cdc25从而调节细胞周期进程提供了新的见解。最近,Chk1已显示不仅调节Cdc25A降解,而且还通过磷酸酶羧基末端的磷酸化与多种Cdk复合物相互作用。出乎意料的是,这些作用似乎是对Chk1特异的,而不是对Chk2特异的,这可能解释了最近报道的使用Chk1条件小鼠模型在乳腺中观察到的体内单倍体功能不足表型。

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