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首页> 外文期刊>Cell cycle >Cell cycle dependent degradation of MCAK: evidence against a role in anaphase chromosome movement.
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Cell cycle dependent degradation of MCAK: evidence against a role in anaphase chromosome movement.

机译:细胞周期依赖的MCAK降解:反对后期染色体运动的作用的证据。

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摘要

MCAK, a kinesin related motor protein with microtubule depolymerizing activity, is known to play an important role in spindle assembly and correcting errors in mitotic chromosome alignment. Experiments to determine how cellular levels of the protein are regulated demonstrate that MCAK accumulates during cell cycle progression, reaches a maximum at G(2)/M phase, and is rapidly degraded by the proteasome during mitosis. Immunofluorescence microscopy further indicates that MCAK largely disappears from kinetochores and spindle poles at the metaphase to anaphase transition. A phosphorylated form of MCAK appears during mitosis and seems to be preferentially degraded, but degradation does not appear to depend on Aurora B, a kinase reported to be involved in regulating the error correcting activity of the protein. These studies indicate that MCAK activity is limited during the latter stages of mitosis by protein degradation, and argue against a role for the protein in anaphase chromosome movement.
机译:MCAK是一种与驱动蛋白有关的运动蛋白,具有微管解聚活性,已知在纺锤体组装和校正有丝分裂染色体排列错误中起着重要作用。确定蛋白水平如何调节的实验表明,MCAK在细胞周期进程中积累,在G(2)/ M期达到最大值,并在有丝分裂期间被蛋白酶体迅速降解。免疫荧光显微镜进一步表明,MCAK在过渡期至后期过渡期从动植物和纺锤体极大量消失。 MCAK的磷酸化形式出现在有丝分裂期间,似乎优先降解,但降解似乎不依赖于Aurora B,据报道该激酶参与调节蛋白的纠错活性。这些研究表明,在有丝分裂的后期,蛋白质降解会限制MCAK的活性,并反对该蛋白质在后期染色体运动中的作用。

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