The p130 pocket protein: keeping order at cell cycle exit/re-entrance transitions.
The p130 pocket protein: keeping order at cell cycle exit/re-entrance transitions.
复制标题
DOI：
10.2741/a263
复制
发表时间：
1998
期刊：
影响因子：
--
通讯作者：
X. Mayol;X. Graña
中科院分区：
文献类型：
--
作者：
X. Mayol;X. Graña
口袋蛋白，包括视网膜母细胞瘤易感基因产物（pRB）和相关蛋白p107和p130，在细胞周期调控步骤中起作用，将细胞周期蛋白/ cdk整合的正、负生长信号与细胞周期进程所需基因上的E2F转录因子活性联系起来。口袋蛋白与转录因子家族E2F成员之间形成的蛋白质复合物决定了E2F复合物是作为转录激活因子还是抑制因子。过去几年的实验工作表明，在不同的细胞生长条件下，单个口袋蛋白与特定的E2F成员相互作用，调节某些基因的转录。在这些蛋白关联中，含有p130的E2F复合物似乎在通过抑制一组E2F应答基因的转录来控制静止和分化细胞中的基因转录方面具有特别重要的作用。一旦细胞进入细胞周期的G1期，口袋蛋白介导的E2F活性调控由pRB和p107承担。因此，p130介导的转录调控似乎阻止了细胞周期退出和再进入过渡和静止细胞中分裂细胞的基因表达程序特征。
Pocket proteins, including the retinoblastoma susceptibility gene product (pRB) and the related proteins p107 and p130, function at cell cycle regulatory steps that link cyclin/CDK-integrated positive and negative growth signals with E2F transcription factor activity on genes required for cell cycle progression. Protein complex formation between pocket proteins and members of the E2F family of transcription factors determines whether E2F complexes act as transcriptional activators or repressors. Experimental work over the last few years indicates that individual pocket proteins interact with specific E2F members to regulate the transcription of certain genes under diverse cell growth conditions. Among these protein associations, p130-containing E2F complexes seem to be of particular importance in controlling gene transcription in quiescent and differentiating cells by repressing the transcription of a set of E2F-responsive genes. Once the cells are progressing through the G1 phase of the cell cycle, pocket protein-mediated regulation of E2F activity is assumed by pRB and p107. p130-mediated transcriptional regulation thus seems to prevent a gene expression program characteristic of dividing cells at the cell cycle exit and re-entrance transitions and in quiescent cells.