E2F4 and E2F5 play an essential role in pocket protein-mediated G1 control
E2F4 and E2F5 play an essential role in pocket protein-mediated G1 control
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DOI：
10.1016/s1097-2765(00)00071-x
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发表时间：
2000-09-01
期刊：
影响因子：
16
通讯作者：
Rempel, RE
中科院分区：
文献类型：
--
作者：
Gaubatz, S;Lindeman, GJ;Rempel, RE
E2F转录因子是细胞增殖的主要调节因子。E2F家族的多样性表明，单个成员在细胞周期控制中发挥着不同的功能。E2F4和E2F5构成该家族的一个定义子集。到目前为止，人们对它们各自的生化和生物学功能知之甚少。在这里，我们报告了E2F4和E2F5在小鼠体内同时失活会导致新生儿死亡，这表明它们在小鼠发育过程中发挥着重叠的功能。与野生型细胞相比，从这些小鼠分离的胚胎成纤维细胞正常增殖，并以正常的动力学从GO进入。然而，它们未能在G1对p16(INK4a)做出反应。因此，E2F4和E2F5对于细胞周期进程是不必要的，但对于口袋蛋白介导的周期细胞G1期停滞是必要的。
E2F transcription factors are major regulators of cell proliferation. The diversity of the E2F family suggests that individual members perform distinct functions in cell cycle control. E2F4 and E2F5 constitute a defined subset of the family. Until now, there has been little understanding of their individual biochemical and biological functions. Here, we report that simultaneous inactivation of E2F4 and E2F5 in mice results in neonatal lethality, suggesting that they perform overlapping functions during mouse development. Embryonic fibroblasts isolated from these mice proliferated normally and reentered from Go with normal kinetics compared to wild-type cells. However, they failed to arrest in G1 in response to p16(INK4a). Thus, E2F4 and E2F5 are dispensable for cell cycle progression but necessary for pocket protein-mediated G1 arrest of cycling cells.