7SK小核RNA与CDK9/环林T复合体结合并抑制其活性
V T Nguyen1, T Kiss, A A Michels
1Génétique Moléculaire, UMR 8541 CNRS, Ecole Normale Supérieure, 46 rue d'Ulm, 75230 Paris cedex 05, France.
Nature
|November 20, 2001
概括
一个新发现的综合体,涉及P-TEFb和7SKRNA,调节RNA聚合酶II的活性. 这种复合物封存P-TEFb,减少其激酶活性,直到转录被抑制,这表明一个反机制.
科学领域:
- 分子生物学分子生物学
- 基因法规 基因法规
- 生物化学 生物化学
背景情况:
- 细胞基因转录是由RNA聚合酶II (Pol II) 活动调节的.
- 通过P-TEFb对Pol II CTD的酸化对于转录延长至关重要.
- P-TEFb由CDK9和环素T1或T2组成.
研究的目的:
- 为了研究P-TEFb活动的调节.
- 为了确定与P-TEFb.交互的新型因素.
- 了解7SKRNA在转录调节中的作用.
主要方法:
- 细胞分离和从人类HeLa细胞中复杂的分离.
- 生物化学试验测量酶活性.
- 在各种条件下分析P-TEFb/7SK复合体的形成和破坏.
主要成果:
- 超过一半的细胞P-TEFb存在于具有7SKRNA的大型复合体中.
- 这些大型7SK/P-TEFb复合体与自由P-TEFb相比,具有显著较低的CDK9激酶活性.
- 转录的抑制导致7SK/P-TEFb复合体的破坏和CDK9活动的增加.
结论:
- 7SKRNA封存P-TEFb,形成一个不活跃的复合体,调节RNA Pol II活动.
- P-TEFb/7SK相互作用代表了一个依赖转录的反机制.
- 这一发现揭示了真核生物基因转录的新型调节途径.
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