Translational control of p27(Kip1) accumulation during the cell cycle
Translational control of p27(Kip1) accumulation during the cell cycle
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DOI：
10.1126/science.271.5257.1861
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发表时间：
1996-03-29
期刊：
影响因子：
56.9
通讯作者：
Reed, SI
中科院分区：
文献类型：
--
作者：
Hengst, L;Reed, SI
真核细胞中的细胞周期相变是由称为细胞周期蛋白依赖性激酶（Cdks）的蛋白激酶的活性调节驱动的。与28千道尔顿蛋白质（p28（lck1））相关的广谱Cdk抑制活性在用药物洛伐他汀处理的细胞中或在密度介导的生长停滞后被诱导，并且在细胞周期中是周期性的，在G（1）中具有峰值活性。p28（lck1）蛋白被证明是相同的p27（Kip1），和周期性或诱导的抑制活性导致的蛋白质的周期性积累。p27蛋白的量发生变化，而p27信使RNA的丰度保持不变。在每一种情况下，p27蛋白水平的转录后改变是通过翻译控制机制的一部分，虽然在密度逮捕的成纤维细胞和胸腺嘧啶逮捕的HeLa细胞的蛋白质的半衰期也发生了变化。
Cell cycle phase transitions in eukaryotic cells are driven by regulation of the activity of protein kinases known as cyclin-dependent kinases (Cdks). A broad spectrum Cdk-inhibitory activity associated with a 28-kilodalton protein (p28(lck1)) was induced in cells treated with the drug lovastatin or upon density-mediated growth arrest and was periodic in the cell cycle, with peak activity in G(1). The p28(lck1) protein was shown to be identical to p27(Kip1), and the periodic or induced inhibitory activity resulted from a periodic accumulation of the protein. Variations in the amount of p27 protein occurred, whereas the abundance of the p27 messenger RNA remained unchanged. In every instance investigated, the posttranscriptional alteration of p27 protein levels was achieved in part by a mechanism of translational control, although in density-arrested fibroblasts and thymidine-arrested HeLa cells the half-life of the protein was also changed.