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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >REGULATION OF E2F THROUGH UBIQUITIN-PROTEASOME-DEPENDENT DEGRADATION - STABILIZATION BY THE PRB TUMOR SUPPRESSOR PROTEIN
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REGULATION OF E2F THROUGH UBIQUITIN-PROTEASOME-DEPENDENT DEGRADATION - STABILIZATION BY THE PRB TUMOR SUPPRESSOR PROTEIN

机译：PRB肿瘤抑制蛋白通过泛素依赖于蛋白质的降解-稳定化调控E2F

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摘要

The E2F family of transcription factors plays a key role in regulating cell-cycle progression, Accordingly, E2F is itself tightly controlled by a series of transcriptional and posttranscriptional events, Here we provide evidence that E2F1 protein levels are regulated by the ubiquitin-proteasome-dependent degradation pathway, An analysis of E2F1 mutants identified a conserved carboxyl-terminal region, which is required for eliciting ubiquitination and protein turnover, Fusion of this E2F1 carboxyl-terminal sequence to a heterologous protein, GAL4, resulted in destabilization of GAL4. Previous studies identified an overlapping region of E2F1 that facilitates complex formation with retinoblastoma tumor suppressor protein, pRB, and we found that pRB blocks ubiquitination and stabilizes E2F1, These results suggest a new mechanism for controlling the cell-cycle regulatory activity of E2F1. [References: 35]
机译：E2F家族的转录因子在调节细胞周期进程中起着关键作用，因此，E2F本身受到一系列转录和转录后事件的严格控制，在这里我们提供证据表明E2F1蛋白水平受泛素-蛋白酶体依赖性调节降解途径，对E2F1突变体的分析确定了保守的羧基末端区域，这是引发泛素化和蛋白质更新所必需的，此E2F1羧基末端序列与异源蛋白质GAL4融合导致GAL4不稳定。先前的研究确定了E2F1的重叠区域，该区域促进与视网膜母细胞瘤肿瘤抑制蛋白pRB的复杂形成，并且我们发现pRB阻断泛素化并稳定E2F1。这些结果提示了一种控制E2F1细胞周期调控活性的新机制。 [参考：35]

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