PI3K is required for insulin-stimulated but not EGF-stimulated ERK1/2 activation
文献类型:期刊论文
作者 | Liu, Lunhua; Xie, Yili; Lou, Liguang![]() |
刊名 | EUROPEAN JOURNAL OF CELL BIOLOGY
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出版日期 | 2006-05 |
卷号 | 85期号:5页码:367-374 |
关键词 | extracellular signal-regulated kinase 1 and 2 phosphatidylinositol 3-kinase insulin epidermal growth factor Ras Akt wortmannin LY294002 protein kinase C phorbol 12-myristate 13-acetate |
ISSN号 | 0171-9335 |
DOI | 10.1016/j.ejcb.2005.11.005 |
文献子类 | Article |
英文摘要 | The Ras/Raf/extracellular signal-regulated kinase I and 2 (ERK1/2) signaling pathway is known to cross-talk with other signaling pathways, including phosphaticlylinositol 3-kinase (PI3K)/Akt pathway. However, the role of PI3K in ERK-1/2 activation induced by tyrosine kinase receptors was not fully understood. Here, we report that two structurally distinct PI3K inhibitors, wortmannin and LY294002, inhibited insulin-induced activation of ERK1/2 but had no effect on EGF-induced activation of ERK1/2 in hepatocellular carcinoma BEL-7402 and SMMC-7721 cells, breast cancer MCF-7 cells, and prostate cancer LNCaP cells. Although protein kinase C could act as a mediator between PI3K and ERK1/2, protein kinase C inhibitor chelerythrine chloride did not inhibit insulin-induced ERK1/2 activation. Both insulin- and EGF-induced ERK1/2 activation are strictly dependent on Ras activation, however, wortmannin only inhibited insulin-induced, but not EGF-induced Ras activation. These results indicate that PI3K plays different roles in the activation of Ras/ERK1/2 signaling by insulin and EGF, and that insulin-stimulated, but not EGF-stimulated, ERK1/2 and Akt signalings diverge at PI3K. (c) 2005 Elsevier GmbH. All rights reserved. |
WOS关键词 | GLYCOGEN-SYNTHASE KINASE-3 ; EPIDERMAL-GROWTH-FACTOR ; PROTEIN-KINASE ; 3T3-L1 ADIPOCYTES ; SIGNALING PATHWAY ; PHOSPHOINOSITIDE 3-KINASE ; GLUCOSE-TRANSPORT ; EXCHANGE FACTOR ; RAT ADIPOCYTES ; C ISOTYPES |
WOS研究方向 | Cell Biology |
语种 | 英语 |
WOS记录号 | WOS:000237616800004 |
出版者 | ELSEVIER GMBH, URBAN & FISCHER VERLAG |
源URL | [http://119.78.100.183/handle/2S10ELR8/273605] ![]() |
专题 | 药理学第一研究室 |
通讯作者 | Lou, Liguang |
作者单位 | Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China |
推荐引用方式 GB/T 7714 | Liu, Lunhua,Xie, Yili,Lou, Liguang. PI3K is required for insulin-stimulated but not EGF-stimulated ERK1/2 activation[J]. EUROPEAN JOURNAL OF CELL BIOLOGY,2006,85(5):367-374. |
APA | Liu, Lunhua,Xie, Yili,&Lou, Liguang.(2006).PI3K is required for insulin-stimulated but not EGF-stimulated ERK1/2 activation.EUROPEAN JOURNAL OF CELL BIOLOGY,85(5),367-374. |
MLA | Liu, Lunhua,et al."PI3K is required for insulin-stimulated but not EGF-stimulated ERK1/2 activation".EUROPEAN JOURNAL OF CELL BIOLOGY 85.5(2006):367-374. |
入库方式: OAI收割
来源:上海药物研究所
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