Myt1:使残基Thr14上的Cdc2磷酸化的wee1型激酶。

A Fattaey, R N Booher
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引用次数: 84

摘要

大多数体细胞分裂周期在DNA合成完成和有丝分裂开始之间包含一个间隙期(G2期)。Cdc2催化亚基atp结合袋内两个保守残基(Thr14和Tyr15)的磷酸化抑制了Cdc2激酶活性,至少在一定程度上控制了有丝分裂进入的延迟。负责这两个磷酸化事件的激酶包括Myt1和Wee1激酶,它们分别磷酸化Cdc2的Thr14和Tyr15。在这个讨论中,我们总结了我们目前对Myt1激酶及其在g2到-M阶段对Cdc2激酶活性的调节的了解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Myt1: a Wee1-type kinase that phosphorylates Cdc2 on residue Thr14.

Most somatic cell division cycles contain a gap period (G2 phase) between the completion of DNA synthesis and the initiation of mitosis. This delay of mitotic entry is controlled, at least in part, by the repression of Cdc2 kinase activity by the phosphorylation of two conserved residues (Thr14 and Tyr15) within the ATP-binding pocket of the Cdc2 catalytic subunit. The kinases responsible for these two phosphorylation events include the Myt1 and Wee1 kinases, which phosphorylate Cdc2 on Thr14 and Tyr15, respectively. In this discussion, we summarise our current knowledge of the Myt1 kinase and its regulation of Cdc2 kinase activity during the G2-to -M phase transition.

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