Insulin Differentially Regulates SAPKs/JNKs and ERKs in CHO Cells Overexpressing Human Insulin Receptors-Reference-Cited by-同舟云学术

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Insulin Differentially Regulates SAPKs/JNKs and ERKs in CHO Cells Overexpressing Human Insulin Receptors

Published:1998-02 Issue:3 Volume:243 Page:765-770
ISSN:0006-291X
Container-title:Biochemical and Biophysical Research Communications
language:en
Short-container-title:Biochemical and Biophysical Research Communications

Author:

Desbois-Mouthon Christèle,Blivet-Van Eggelpoel Marie-José,Auclair Martine,Cherqui Gisèle,Capeau Jacqueline,Caron Martine

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

Reference50 articles.

1. The insulin signalling system and the IRS proteins

2. Mitogenic properties of insulin and insulin analogues mediated by the insulin receptor

3. Involvement of Shc in insulin- and epidermal growth factor-induced activation of p21ras.

4. Shc is the predominant signaling molecule coupling insulin receptors to activation of guanine nucleotide releasing factor and p21ras-GTP formation.

5. Insulin receptor substrate-1 (IRS1) and Shc compete for a limited pool of Grb2 in mediating insulin downstream signaling.

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4. Differential regulation of CIDEA and CIDEC expression by insulin via Akt1/2- and JNK2-dependent pathways in human adipocytes;Journal of Lipid Research;2011-08

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