Cyclin C/Cdk3 promotes Rb-dependent G0 exit
Cyclin C/Cdk3 promotes Rb-dependent G0 exit
复制标题
DOI：
10.1016/s0092-8674(04)00300-9
复制
发表时间：
2004-04-16
期刊：
影响因子：
64.5
通讯作者：
Rollins, BJ
中科院分区：
文献类型：
--
作者：
Ren, SJ;Rollins, BJ
G 0是由已经退出细胞周期的静息或终末分化细胞占据的生理状态。与控制G1/S转换的细胞周期蛋白/cdk介导的pRb失活相反，对G 0/G1转换的调节知之甚少。然而，pRb可能参与这一过程，因为其急性体细胞失活足以使G 0期阻滞的细胞重新进入细胞周期。该事件的一个生理调节因子可能是细胞周期蛋白C，因为其最高mRNA水平发生在G 0退出期间。在这里，我们表明，一个非cdk 8相关的细胞池的细胞周期蛋白C结合cdk 3刺激pRb磷酸化在S807/811在G 0/G1过渡期间，这种磷酸化是必需的细胞退出G 0有效。因此，G1期进入以类似于S期进入的方式调节，但涉及不同的细胞周期蛋白/cdk组合。
G0 is a physiological state occupied by resting or terminally differentiated cells that have exited the cell cycle. In contrast to the well-characterized cyclin/cdk-mediated inactivation of pRb that controls the G1/S transition, little is known about regulation of the G0/G1 transition. However, pRb is likely to participate in this process because its acute somatic inactivation is sufficient for G0-arrested cells to reenter the cell cycle. One physiological regulator of this event may be cyclin C because its highest mRNA levels occur during G0 exit. Here we show that a non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and that this phosphorylation is required for cells to exit G0 efficiently. Thus, G1 entry is regulated in an analogous fashion to S phase entry, but involves a distinct cyclin/cdk combination.