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含TBP的因子SL1的有丝分裂磷酸化抑制核糖体基因转录。

Mitotic phosphorylation of the TBP-containing factor SL1 represses ribosomal gene transcription.

作者信息

Kuhn A, Vente A, Dorée M, Grummt I

机构信息

German Cancer Research Center, Heidelberg, D-69120, Germany.

出版信息

J Mol Biol. 1998 Nov 20;284(1):1-5. doi: 10.1006/jmbi.1998.2164.

Abstract

Entry into mitosis is accompanied by a global repression of transcription. To investigate the molecular mechanisms which shut-down rRNA synthesis during mitosis, we have compared RNA polymerase I (Pol I) transcription in extracts from asynchronous and mitotic HeLa cells. We show by several experimental approaches that phosphorylation by cdc2/cyclin B inactivates the TBP-containing factor SL1 and thus abrogates Pol I transcription during mitosis. This finding links the cell's cycle with the transcriptional activity of Pol I and suggests a common mechanism for mitotic silencing of all three classes of nuclear RNA polymerases, i.e. reversible inactivation of the respective TBP-TAF complexes by (a) mitotic kinase(s).

摘要

进入有丝分裂伴随着转录的全面抑制。为了研究在有丝分裂期间关闭rRNA合成的分子机制,我们比较了来自异步和有丝分裂期HeLa细胞提取物中的RNA聚合酶I(Pol I)转录。我们通过几种实验方法表明,cdc2/细胞周期蛋白B介导的磷酸化使含TBP的因子SL1失活,从而在有丝分裂期间消除Pol I转录。这一发现将细胞周期与Pol I的转录活性联系起来,并提示了所有三类核RNA聚合酶有丝分裂沉默的共同机制,即通过一种(或多种)有丝分裂激酶使各自的TBP-TAF复合物可逆失活。

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