Role of ERK1/ERK2 and p70S6K pathway in insulin signalling of protein synthesis

被引：13

作者：

Sale, EM ^{[1
]}

Atkinson, PPG ^{[1
]}

Arnott, CH ^{[1
]}

Chad, JE ^{[1
]}

Sale, GJ ^{[1
]}

机构：

[1] Sch Biol Sci, Div Biochem & Mol Biol, Southampton SO16 7PX, Hants, England

来源：

FEBS LETTERS | 1999年 / 446卷 / 01期

关键词：

insulin; protein synthesis; extracellular signal regulated kinase 1; extracellular signal regulated kinase 2; p70(S6K); antisense;

D O I：

10.1016/S0014-5793(99)00193-3

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The signalling pathways by which insulin triggers protein synthesis were studied using an antisense strategy to deplete ERK1/ERK2 and rapamycin to inhibit the p70(S6K) pathway. The results indicated that ERK1/ERK2 principally regulated the amount of the protein synthesis machinery available in the cell while the p70(S6K) pathway contributed to modulating its activation in response to insulin, ERK1/ERK2 also mediated in a small proportion of insulin-stimulated protein synthesis which included the induction of c-fos protein. When c-fos induction was blocked the majority of insulin-stimulated protein synthesis still occurred and thus did not require transcriptional regulation of c-fos or its targets. (C) 1999 Federation of European Biochemical Societies.

引用

页码：122 / 126

页数：5

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