Cooperation between the Cdk inhibitors p27(KIP1) and p57(KIP2) in the control of tissue growth and development.
Cooperation between the Cdk inhibitors p27(KIP1) and p57(KIP2) in the control of tissue growth and development.
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DOI：
10.1101/gad.12.20.3162
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发表时间：
1998-10
影响因子：
10.5
通讯作者：
Pumin Zhang;C. Wong;R. DePinho;J. Harper;S. Elledge
中科院分区：
文献类型：
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作者：
Pumin Zhang;C. Wong;R. DePinho;J. Harper;S. Elledge
细胞周期退出是许多细胞类型终末分化所必需的。视网膜母细胞瘤蛋白Rb在几种组织中参与细胞周期退出和分化。Rb受细胞周期蛋白依赖性激酶（Cdks）负调控。在透镜或其他组织中下调Cdk活性以激活Rb的主要效应物尚不清楚。在这项研究中，使用多个突变小鼠，我们表明，Cdk抑制剂p27（KIP 1）和p57（KIP 2）冗余功能控制细胞周期退出和分化的透镜纤维细胞和胎盘滋养层细胞。这些研究表明，p27（KIP1）和p57（KIP2）是控制细胞分化的信号转导途径的关键终端效应器。
Cell cycle exit is required for terminal differentiation of many cell types. The retinoblastoma protein Rb has been implicated both in cell cycle exit and differentiation in several tissues. Rb is negatively regulated by cyclin-dependent kinases (Cdks). The main effectors that down-regulate Cdk activity to activate Rb are not known in the lens or other tissues. In this study, using multiple mutant mice, we show that the Cdk inhibitors p27(KIP1) and p57(KIP2) function redundantly to control cell cycle exit and differentiation of lens fiber cells and placental trophoblasts. These studies demonstrate that p27(KIP1) and p57(KIP2) are critical terminal effectors of signal transduction pathways that control cell differentiation.