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. 2005 Sep 30;335(3):836-42.
doi: 10.1016/j.bbrc.2005.07.152.

Roles of mTOR and JNK in serine phosphorylation, translocation, and degradation of IRS-1

Kazuyuki Hiratani  1 , Tetsuro Haruta, Akihiro Tani, Junko Kawahara, Isao Usui, Masashi Kobayashi
Affiliations

Roles of mTOR and JNK in serine phosphorylation, translocation, and degradation of IRS-1

Kazuyuki Hiratani et al. Biochem Biophys Res Commun. .

Abstract

In 3T3-L1 adipocytes, insulin or anisomycin stimulated phosphorylation of IRS-1 at Ser(307) and Ser(636/639), both of which were partially reduced by the mTOR inhibitor, rapamycin, or the JNK inhibitor, SP600125, and were further inhibited by a combination of them. Interestingly, anisomycin-induced p70(S6K) phosphorylation was reduced by SP600125, while insulin-induced p70(S6K) phosphorylation was not. Furthermore, unlike insulin, anisomycin failed to elicit translocation or degradation of IRS-1. These results indicate that mTOR and JNK play roles in phosphorylating IRS-1 serine residues, and that insulin and anisomycin are different in terms of the relationship of activation between mTOR and JNK, and the effects on IRS-1 localization and stability.

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