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Transcription elongation control by the 7SK snRNP complex: Releasing the pause

机译:7SK snRNP复合体控制转录延伸:消除暂停

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摘要

The ability for the eukaryotic cell to transcriptionally respond to various stimuli is critical for the overall homeostasis of the cell, and in turn, the organism. The human RNA polymerase II complex (Pol II), which is responsible for the transcription of protein-encoding genes and non-coding RNAs, is paused at promoter-proximal regions to ensure their rapid activation. In response to stimulation, Pol II pause release is facilitated by the action of positive transcription elongation factors such as the P-TEFb kinase. However, the majority of P-TEFb is held in a catalytically inactivate state, assembled into the 7SK small nuclear ribonucleoprotein (snRNP) complex, and must be dislodged to become catalytically active. In this review, we discuss mechanisms of 7SK snRNP recruitment to promoter-proximal regions and P-TEFb disassembly from the inhibitory snRNP to regulate on site' kinase activation and Pol II pause release.
机译:真核细胞对各种刺激转录应答的能力对于细胞乃至生物体的整体稳态至关重要。负责蛋白质编码基因和非编码RNA转录的人类RNA聚合酶II复合物(Pol II)停在启动子附近区域,以确保其快速激活。响应刺激,通过正转录伸长因子(例如P-TEFb激酶)的作用促进Pol II暂停释放。但是,大多数P-TEFb处于催化失活状态,组装成7SK小核核糖核蛋白(snRNP)复合物,必须去除后才能具有催化活性。在这篇综述中,我们讨论了7SK snRNP募集到启动子附近区域的机制以及P-TEFb从抑制性snRNP拆卸来调节现场激酶激活和Pol II暂停释放的机制。

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