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Sci STKE. 2005 Jan 25;2005(268):pe4.

Ser/Thr phosphorylation of IRS proteins: a molecular basis for insulin resistance.

Author information

  • 1Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel. yehiel.zick@weizmann.ac.il <yehiel.zick@weizmann.ac.il>

Abstract

S6K1, like other serine and threonine kinases activated by insulin (such as mTOR and PKCzeta), has recently been shown to participate in negative feedback mechanisms aimed at terminating insulin signaling through IRS (insulin receptor substrate) phosphorylation. Such homeostatic mechanisms can also be activated by excess nutrients or inducers of insulin resistance (such as fatty acids and proinflammatory cytokines) to produce an insulin-resistant state that often leads to the development of diabetes. Identification of the specific kinases involved in such insulin resistance pathways can help lead to the rational design of novel therapeutic agents for treating insulin resistance and type 2 diabetes.

PMID:
15671481
DOI:
10.1126/stke.2682005pe4
[PubMed - indexed for MEDLINE]
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