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J Biol Chem, Vol. 275, Issue 12, 9047-9054, March 24, 2000
From the Howard Hughes Medical Institute, Joslin Diabetes Center,
Harvard Medical School, Boston, Massachusetts 02215 and ¶ Howard
Hughes Medical Institute, Department of Molecular Medicine, University
of Massachusetts, Worcester, Massachusetts 01605
Tumor necrosis factor
The c-Jun NH2-terminal Kinase Promotes Insulin
Resistance during Association with Insulin Receptor Substrate-1 and
Phosphorylation of Ser307*
,
(TNF) inhibits
insulin action, in part, through serine phosphorylation of IRS
proteins; however, the phosphorylation sites that mediate the
inhibition are unknown. TNF promotes multipotential signal
transduction cascades, including the activation of the Jun
NH2-terminal kinase (JNK). Endogenous JNK associates
with IRS-1 in Chinese hamster ovary cells. Anisomycin, a strong
activator of JNK in these cells, stimulates the activity of JNK bound
to IRS-1 and inhibits the insulin-stimulated tyrosine phosphorylation
of IRS-1. Serine 307 is a major site of JNK phosphorylation in IRS-1.
Mutation of serine 307 to alanine eliminates phosphorylation of IRS-1
by JNK and abrogates the inhibitory effect of TNF on insulin-stimulated tyrosine phosphorylation of IRS-1. These results suggest that phosphorylation of serine 307 might mediate, at least partially, the inhibitory effect of proinflammatory cytokines like
TNF on IRS-1 function.
*
This work was supported by DK38712 (to M. F. W.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by an American Diabetes Association Mentor-based Fellowship.
§
Present address: Dept. de Bioquimica I Biologia Molecular, Facultat
de Ciencies Biologiques, 46100-Burjassot, Valencia, Spain.
To whom correspondence should be addressed: Howard Hughes
Medical Institute, Joslin Diabetes Center, 1 Joslin Pl., Boston, MA
02215. Tel.: 617-732-2578; Fax: 617-732-2593; E-mail:
morris.white@joslin.harvard.edu.
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