细胞周期蛋白与G2/M转变。

Cancer surveys Pub Date : 1997-01-01
M R Jackman, J N Pines
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引用次数: 0

摘要

细胞进入有丝分裂是由一个精细的激酶和磷酸酶网络调控的,它们控制着细胞分裂的时间和细胞结构的完全重组。有丝分裂周期蛋白/Cdks构成了大型多蛋白复合物的一部分,其其他成分现在才开始被识别。对促成这些复合体的蛋白质的持续鉴定和这些复合体组成的变化,可能会对有丝分裂周期蛋白/Cdk复合体是如何被调节的以及它们是如何起作用的——不仅是诱导有丝分裂,而且还有助于进一步的有丝分裂进程——提供一个更综合的观点。此外,将特定的G2/M功能分配给不同的有丝分裂周期蛋白/Cdk复合物将需要鉴定有丝分裂周期蛋白/Cdk复合物之间底物特异性的差异,可能与小鼠中特定的细胞周期蛋白敲除平行。体外和体内有丝分裂周期蛋白/Cdk复合物的潜在功能重叠将使此类研究变得复杂。虽然细胞周期蛋白/Cdk1被认为是启动有丝分裂的主要激酶,但要更全面地了解细胞如何从G2进入有丝分裂状态,还需要进一步鉴定与Cdk1并行的上游、下游激酶、它们的底物以及它们在G2/M转变过程中的相互关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cyclins and the G2/M transition.

The entry of a cell into mitosis is regulated by an elaborate network of kinases and phosphatases that control both for the timing of cell division and the complete reorganization of the cellular architecture. The mitotic cyclin/Cdks form part of large multiprotein complexes whose other components are only now beginning to be identified. The continuing identification of proteins that contribute to these complexes and changes in the composition of these complexes are likely to give a more integrated view of how mitotic cyclin/Cdk complexes are regulated and how they function-not only to induce mitosis, but also to aid further mitotic progression. Furthermore, assigning specific G2/M functions to distinct mitotic cyclin/Cdk complexes will require the identification of differences in substrate specificities between the mitotic cyclin/Cdk complexes, perhaps in parallel with specific cyclin knockouts in mice. Such investigations will be complicated by potential functional overlap between mitotic cyclin/Cdk complexes in vitro and in vivo. Although cyclin/Cdk1 is thought to be the major kinase that initiates the onset of mitosis, a more complete understanding of how cells move from G2 to a mitotic state will require further identification of kinases operating upstream, downstream and in parallel with Cdk1, their substrates and their relationship with one another during the G2/M transition.

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