Suppr超能文献

pp70核糖体蛋白S6激酶与3T3-L1脂肪细胞中胰岛素刺激的葡萄糖转运的解离

Dissociation of pp70 ribosomal protein S6 kinase from insulin-stimulated glucose transport in 3T3-L1 adipocytes.

作者信息

Fingar D C, Hausdorff S F, Blenis J, Birnbaum M J

机构信息

Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115.

出版信息

J Biol Chem. 1993 Feb 5;268(4):3005-8.

PMID:7679106
Abstract

The metabolic and mitogenic actions of insulin have been proposed to be mediated by cellular serine/threonine kinases such as the ribosomal protein S6 kinases pp70-S6 (pp70-S6 kinase) and pp90rsk and the erk-encoded mitogen-activated protein kinases (pp42mapk and pp44mapk). Rapamycin completely blocked activation of pp70-S6 kinase by insulin in 3T3-L1 adipocytes, but did not inhibit insulin-stimulated glucose transport, translocation of GLUT4 to the cell surface, or activation of pp90rsk or pp44mapk by insulin. Concordant with the inhibition of kinase activity, rapamycin prevented the insulin-induced decrease in mobility of pp70-S6 kinase visualized by SDS-polyacrylamide gel electrophoresis, reflecting a reduction in the hormone-stimulated phosphorylation of the enzyme. The structurally related macrolide, FK506, had no effect on pp70-S6 kinase or hexose uptake. These data demonstrate that rapamycin blocks insulin activation of pp70-S6 kinase in 3T3-L1 adipocytes and that pp70-S6 kinase is not required in the signaling pathway leading to insulin-stimulated glucose transport.

摘要

胰岛素的代谢和促有丝分裂作用被认为是由细胞丝氨酸/苏氨酸激酶介导的,如核糖体蛋白S6激酶pp70-S6(pp70-S6激酶)、pp90rsk以及erk编码的丝裂原活化蛋白激酶(pp42mapk和pp44mapk)。雷帕霉素完全阻断了胰岛素对3T3-L1脂肪细胞中pp70-S6激酶的激活,但不抑制胰岛素刺激的葡萄糖转运、GLUT4向细胞表面的转位,或胰岛素对pp90rsk或pp44mapk的激活。与激酶活性的抑制相一致,雷帕霉素阻止了胰岛素诱导的pp70-S6激酶迁移率降低,这通过SDS-聚丙烯酰胺凝胶电泳可见,反映了激素刺激的该酶磷酸化减少。结构相关的大环内酯类药物FK506对pp70-S6激酶或己糖摄取没有影响。这些数据表明,雷帕霉素阻断了3T3-L1脂肪细胞中胰岛素对pp70-S6激酶的激活,并且在导致胰岛素刺激的葡萄糖转运的信号通路中不需要pp70-S6激酶。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验