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Ha-ras基因的第12位缬氨酸突变为甘氨酸、第59位苏氨酸突变为丝氨酸,在非洲爪蟾卵母细胞中激活S6激酶和p34cdc2激酶:c-mos依赖和非依赖途径的证据

Ha-rasVal-12,Thr-59 activates S6 kinase and p34cdc2 kinase in Xenopus oocytes: evidence for c-mosxe-dependent and -independent pathways.

作者信息

Barrett C B, Schroetke R M, Van der Hoorn F A, Nordeen S K, Maller J L

机构信息

Department of Pharmacology, University of Colorado School of Medicine, Denver 80262.

出版信息

Mol Cell Biol. 1990 Jan;10(1):310-5. doi: 10.1128/mcb.10.1.310-315.1990.

Abstract

Treatment with insulin or progesterone or microinjection of the transforming protein product of Ha-rasVal-12,Thr-59 (p21) is known to induce germinal vesicle breakdown in Xenopus oocytes. We have investigated the effect of p21 on S6 kinase and the H1 histone kinase of maturation-promoting factor in the presence and absence of antisense oligonucleotides against the c-mosxe proto-oncogene. Injection of p21 led to a rapid increase in S6 phosphorylation, with kinetics similar to those previously observed with insulin. Microinjection of c-mosxe antisense oligonucleotides inhibited germinal vesicle breakdown induced by p21 and totally abolished S6 kinase activation by insulin or progesterone but only partially inhibited activation by p21. However, the activation of p34cdc2 protein kinase by all three stimuli was blocked by antisense oligonucleotides. The results suggest that in oocyte maturation c-mosxe functions downstream of p21 but upstream of p34cdc2 and S6 kinase activation, although not all p21-induced events require c-mosxe.

摘要

已知用胰岛素或孕酮处理或显微注射Ha-rasVal-12、Thr-59(p21)的转化蛋白产物可诱导非洲爪蟾卵母细胞的生发泡破裂。我们研究了在有和没有针对c-mosxe原癌基因的反义寡核苷酸存在的情况下,p21对S6激酶和成熟促进因子的H1组蛋白激酶的影响。注射p21导致S6磷酸化迅速增加,其动力学与先前用胰岛素观察到的相似。显微注射c-mosxe反义寡核苷酸可抑制p21诱导的生发泡破裂,并完全消除胰岛素或孕酮对S6激酶的激活,但仅部分抑制p21的激活。然而,所有三种刺激对p34cdc2蛋白激酶的激活均被反义寡核苷酸阻断。结果表明,在卵母细胞成熟过程中,c-mosxe在p21的下游但在p34cdc2和S6激酶激活的上游发挥作用,尽管并非所有p21诱导的事件都需要c-mosxe。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a654/360742/40d78f246b37/molcellb00037-0332-a.jpg

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