The protein kinase p90 Rsk as an essential mediator of cytostatic factor activity
The protein kinase p90 Rsk as an essential mediator of cytostatic factor activity
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DOI：
10.1126/science.286.5443.1362
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发表时间：
1999-11-12
期刊：
影响因子：
56.9
通讯作者：
Ferrell, JE
中科院分区：
文献类型：
--
作者：
Bhatt, RR;Ferrell, JE
在有丝分裂过程中p42丝裂原活化蛋白激酶（p42 MAPK）的持续激活诱导了一种“细胞生长抑制因子”阻滞，这种阻滞负责防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。非洲爪蟾卵提取物的免疫耗竭RSK失去了他们的能力，进行有丝分裂停滞的Mos-MEK-1-p42 MAPK级联的蛋白激酶的激活。补充RSK耗尽提取物与催化活性RSK蛋白恢复的提取物进行有丝分裂阻滞的能力。Rsk似乎是必不可少的细胞生长抑制因子逮捕。
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.