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Insulin differentially regulates SAPKs/JNKs and ERKs in CHO cells overexpressing human insulin receptors.

作者信息

Desbois-Mouthon C, Blivet-Van Eggelpoel M J, Auclair M, Cherqui G, Capeau J, Caron M

机构信息

INSERM U.402, Faculté de Médecine Saint-Antoine, Paris, France.

出版信息

Biochem Biophys Res Commun. 1998 Feb 24;243(3):765-70. doi: 10.1006/bbrc.1998.8181.

DOI:10.1006/bbrc.1998.8181
PMID:9501008
Abstract

In the present study, we compared the ability of insulin to regulate SAPKs/JNKs and ERKs in CHO cells overexpressing human insulin receptors. We show that acute insulin treatment induced a time-dependent increase both in SAPK/JNK and ERK activity but with distinct kinetics. PI-3-kinase inhibition by wortmannin completely blocked insulin activation of SAPKs/JNKs, whereas it partially decreased ERK activation. Prolonged exposure to insulin caused a marked inhibition of SAPK/JNK activity while it induced a sustained activation of ERKs. Insulin inhibition of SAPKs/JNKs was partly due to decreased tyrosine phosphorylation of JNK2. These data indicate that insulin differentially regulates SAPKs/JNKs and ERKs. Moreover, they provide the first evidence that insulin exerts opposite effects on SAPK/JNK activity according to the time of cell treatment.

摘要

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