...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >E2F4 Is Exported from the Nucleus in a CRM1-Dependent Manner
【24h】

E2F4 Is Exported from the Nucleus in a CRM1-Dependent Manner

机译：E2F4以依赖CRM1的方式从核中导出

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

E2F is a family of transcription factors required for normal cell cycle control and for cell cycle arrest in G1. E2F4 is the most abundant E2F protein in many cell types. In quiescent cells, it is localized to the nucleus, where it is bound to the retinoblastoma-related protein p130. During entry into the cell cycle, the protein disappears from the nucleus and appears in the cytoplasm. The mechanism by which this change occurs has, in the past, been unclear. We have found that E2F4 is actively exported from the nucleus and that leptomycin B, a specific inhibitor of nuclear export, inhibits this process. E2F4 export is mediated by two hydrophobic export sequences, mutations in either of which result in export failure. Individual export mutants of E2F4, but not a mutant with inactivation of both export signals, can be efficiently excluded from the nucleus by forced coexpression of the nuclear export receptor CRM1. Similarly, CRM1 overexpression can prevent cell cycle arrest induced by the cyclin kinase inhibitor p16INK4a, an E2F4-dependent process. Taken together, these data suggest that nuclear export contributes to the regulation of E2F4 function, including its ability to regulate exit from G1 in association with a suitable pocket protein.
机译：E2F是正常细胞周期控制和G 1 中细胞周期停滞所需的转录因子家族。 E2F4是许多细胞类型中最丰富的E2F蛋白。在静态细胞中，它定位于细胞核，并与视网膜母细胞瘤相关蛋白p130结合。在进入细胞周期的过程中，蛋白质从细胞核中消失并出现在细胞质中。过去，这种变化发生的机制尚不清楚。我们发现，E2F4从核中活跃地输出，而瘦核素B（一种核输出的特异性抑制剂）抑制了这一过程。 E2F4的输出是由两个疏水性输出序列介导的，其中任何一个突变都会导致输出失败。通过强制共表达核输出受体CRM1，可以有效地将E2F4的单个输出突变体，而不是两个输出信号均失活的突变体从核中有效排除。同样，CRM1过表达可以防止细胞周期蛋白激酶抑制剂p16 INK4a 诱导的细胞周期停滞，这是一种依赖于E2F4的过程。综上所述，这些数据表明核出口有助于E2F4功能的调节，包括其调节G 1 与合适的口袋蛋白结合的能力。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号