An essential role of the JIP1 scaffold protein for JNK activation in adipose tissue

  1. Anja Jaeschke1,2,
  2. Michael P. Czech2, and
  3. Roger J. Davis1,2,3
  1. 1Howard Hughes Medical Institute and 2Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA

Abstract

The c-Jun NH2-terminal kinase (JNK) is activated during obesity. One consequence of obesity is that JNK phosphorylates the adapter protein insulin receptor substrate 1 (IRS-1) on Ser 307 and inhibits signaling by the insulin receptor. JNK can therefore cause peripheral insulin resistance during obesity and may contribute to the development of type 2 diabetes. Here we report that the JNK-interacting protein 1 (JIP1) scaffold protein, which binds components of the JNK signaling module, is essential for JNK activation in the adipose tissue of obese mice. These data identify JIP1 as a novel molecular target for therapeutic intervention in the development of obesity.

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Footnotes

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1216504.

  • ↵3 Corresponding author. E-MAIL Roger.Davis{at}Umassmed.edu; FAX (508) 856-3210.

    • Accepted June 14, 2004.
    • Received April 29, 2004.
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  1. doi: 10.1101/gad.1216504 Genes & Dev. 18: 1976-1980 Cold Spring Harbor Laboratory Press

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