G1 cyclin-dependent kinases are insufficient to reverse dE2F2-mediated repression
G1 cyclin-dependent kinases are insufficient to reverse dE2F2-mediated repression
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DOI：
10.1101/gad.1031803
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发表时间：
2003-03-15
影响因子：
10.5
通讯作者：
Dyson, NJ
中科院分区：
文献类型：
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作者：
Frolov, MV;Stevaux, O;Dyson, NJ
本研究表明，de2f1缺失细胞的细胞周期缺陷依赖于dE2F2和DACAPO （DAP）的协同作用，DACAPO是Cyclin E/cyclindependent kinase 2 （CycE/cdk2）的抑制剂。缺乏dE2F1/dE2F2和dE2F1/DAP的细胞的不同特性导致令人惊讶的观察到，dE2F2介导的抑制不同于视网膜母细胞瘤家族蛋白1 （RBF1）对dE2F1的抑制，并且对CycE/cdk2和Cyclin D/ Cyclin依赖性激酶4 （CycD/cdk4）都有抗性。即使dE2F2/RBF1复合物被CycE/cdk2破坏，这种抗性也会发生，这可能解释了为什么dE2F2在缺乏de2f1的情况下如此有效。这些结果的含义是含有dE2F2的细胞需要dE2F1来阻止或逆转de2f7介导的抑制。
Here we show that the cell cycle defects of dE2F1-depleted cells depend on the cooperative effects of dE2F2 and DACAPO (DAP), an inhibitor of Cyclin E/cyclindependent kinase 2 (CycE/cdk2). The different properties of cells lacking dE2F1/dE2F2 and dE2F1/DAP lead to the surprising observation that dE2F2-mediated repression differs from retinoblastoma family protein 1 (RBF1) inhibition of dE2F1, and is resistant to both CycE/cdk2 and Cyclin D/cyclin-dependent kinase 4 (CycD/cdk4). This resistance occurs even though dE2F2/RBF1 complexes are disrupted by CycE/cdk2, and may explain why dE2F2 is so potent in the absence of de2f1. The implication of these results is that cells containing dE2F2 require dE2F1 to either prevent, or reverse, dE2F7-mediated repression.