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蛋白激酶p90 rsk作为细胞静止因子活性的重要介质。

The protein kinase p90 rsk as an essential mediator of cytostatic factor activity.

作者信息

Bhatt R R, Ferrell J E

机构信息

Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, CA 94305-5332, USA.

出版信息

Science. 1999 Nov 12;286(5443):1362-5. doi: 10.1126/science.286.5443.1362.

Abstract

Persistent activation of p42 mitogen-activated protein kinase (p42 MAPK) during mitosis induces a "cytostatic factor" arrest, the arrest responsible for preventing the parthenogenetic activation of unfertilized eggs. The protein kinase p90 Rsk is a substrate of p42 MAPK; thus, the role of p90 Rsk in p42 MAPK-induced mitotic arrest was examined. Xenopus laevis egg extracts immunodepleted of Rsk lost their capacity to undergo mitotic arrest in response to activation of the Mos-MEK-1-p42 MAPK cascade of protein kinases. Replenishing Rsk-depleted extracts with catalytically competent Rsk protein restored the ability of the extracts to undergo mitotic arrest. Rsk appears to be essential for cytostatic factor arrest.

摘要

在有丝分裂期间,p42丝裂原活化蛋白激酶(p42 MAPK)的持续激活会诱导一种“细胞静止因子”停滞,这种停滞负责阻止未受精卵的孤雌激活。蛋白激酶p90 Rsk是p42 MAPK的底物;因此,研究了p90 Rsk在p42 MAPK诱导的有丝分裂停滞中的作用。用免疫法去除Rsk的非洲爪蟾卵提取物失去了响应Mos-MEK-1-p42 MAPK蛋白激酶级联激活而发生有丝分裂停滞的能力。用具有催化活性的Rsk蛋白补充去除Rsk的提取物可恢复提取物发生有丝分裂停滞的能力。Rsk似乎对细胞静止因子停滞至关重要。

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