Surfing the insulin signaling web

被引：68

作者：

Van Obberghen, E ^{[1
]}

Baron, V ^{[1
]}

Delahaye, L ^{[1
]}

Emanuelli, B ^{[1
]}

Filippa, N ^{[1
]}

Giorgetti-Peraldi, S ^{[1
]}

Lebrun, P ^{[1
]}

Mothe-Satney, I ^{[1
]}

Peraldi, P ^{[1
]}

Rocchi, S ^{[1
]}

Sawka-Verhelle, D ^{[1
]}

Tartare-Deckert, S ^{[1
]}

Giudicelli, J ^{[1
]}

机构：

[1] Fac Med, INSERM, U145, IFR 50, Nice, France

来源：

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION | 2001年 / 31卷 / 11期

关键词：

insulin; IGF-I; insulin/IGF-I receptor; insulin/IGF-I action; tyrosine kinases;

D O I：

10.1046/j.1365-2362.2001.00896.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The diverse biological actions of insulin and insulin-like growth factor I (IGF-I) are initiated by binding of the polypeptides to their respective cell surface tyrosine kinase receptors. These activated receptors phosphorylate a series of endogenous substrates on tyrosine, amongst which the insulin receptor substrate (IRS) proteins are the best characterized. Their phosphotyrosine-containing motifs become binding sites for Src homology 2 (SH2) domains on proteins such as SH2 domain-containing protein-tyrosine-phosphatase (SHP)-2/Syp, growth factor receptor bound-2 protein, (Grb-2), and phosphatidyl inositol 3 kinase (PI3 kinase), which participate in activation of specific signaling cascades. However, the IRS molecules are not only platforms for signaling molecules, they also orchestrate the generation of signal specificity integration of signals induced by several extracellular stimuli, and signal termination and modulation. An extensive review is beyond the scope of the present article, which will be centered on our own contribution and reflect our biases.

引用

页码：966 / 977

页数：12

共 87 条

[1] Early neonatal death in mice homozygous for a null allele of the insulin receptor gene [J].