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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >G1 phase arrest induced by Wilms tumor protein WT1 is abrogated by cyclin/CDK complexes.
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G1 phase arrest induced by Wilms tumor protein WT1 is abrogated by cyclin/CDK complexes.

机译：Wilms肿瘤蛋白WT1诱导的G1期阻滞被细胞周期蛋白/ CDK复合物消除。

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摘要

WT1, the Wilms tumor-suppressor gene, maps to the human chromosomal region 11p13 and encodes a transcriptional repressor, WT1, implicated in controlling normal urogenital development. Microinjection of the WT1 cDNA into quiescent cells or cells in early to mid G1 phase blocked serum-induced cell cycle progression into S phase. The activity of WT1 varied significantly depending on the presence or absence of an alternatively spliced region located upstream of the zinc finger domain. The inhibitory activity of WT1 was abrogated by the overexpression of cyclin E/CDK2 as well as cyclin D1/CDK4. Furthermore, both CDK4- and CDK2-associated kinase activities were downregulated in cells overexpressing WT1, whereas the levels of CDK4, CDK2, and cyclin D1 expression were unchanged. These findings suggest that inhibition of the activity of cyclin/CDK complexes may be involved in mediating the WT1-induced cell cycle block.
机译：WT1是Wilms肿瘤抑制基因，它定位于人类染色体区域11p13，并编码一个转录抑制因子WT1，与控制正常的泌尿生殖道发育有关。将WT1 cDNA微注射到静止细胞或处于G1早期至中期的细胞中可阻止血清诱导的细胞周期进入S期。根据是否存在位于锌指结构域上游的选择性剪接区域，WT1的活性发生显着变化。细胞周期蛋白E / CDK2以及细胞周期蛋白D1 / CDK4的过表达消除了WT1的抑制活性。此外，在过量表达WT1的细胞中，与CDK4和CDK2相关的激酶活性均被下调，而CDK4，CDK2和细胞周期蛋白D1的表达水平未改变。这些发现表明，对细胞周期蛋白/ CDK复合物活性的抑制可能与介导WT1诱导的细胞周期阻滞有关。

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