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The insulin signaling system.

Morris F. White, +1 more
- 07 Jan 1994 - 
- Vol. 269, Iss: 1, pp 1-4
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This article is published in Journal of Biological Chemistry.The article was published on 1994-01-07 and is currently open access. It has received 1696 citations till now. The article focuses on the topics: Insulin Receptor Substrate Proteins & Insulin receptor.

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Citations
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IRS-1-Mediated Inhibition of Insulin Receptor Tyrosine Kinase Activity in TNF-α- and Obesity-Induced Insulin Resistance

TL;DR: Results indicate that TNF-α induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.
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Protection from obesity-induced insulin resistance in mice lacking TNF-|[alpha]| function

TL;DR: Results indicate that TNF-α is an important mediator of insulin resistance in obesity through its effects on several important sites of insulin action.
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Increased insulin sensitivity and obesity resistance in mice lacking the protein tyrosine phosphatase-1B gene.

TL;DR: In this article, the mouse homolog of the gene encoding PTP-1B yielded healthy mice that, in the fed state, had blood glucose concentrations that were slightly lower and concentrations of circulating insulin that were one-half those of their PTP−1B+/+ littermates.
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The ATP Synthase—A Splendid Molecular Machine

TL;DR: An X-ray structure of the F1 portion of the mitochondrial ATP synthase shows asymmetry and differences in nucleotide binding of the catalytic beta subunits that support the binding change mechanism with an internal rotation of the gamma subunit.
References
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Journal ArticleDOI

Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

TL;DR: A role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity is indicated.
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Oncogenes and signal transduction

TL;DR: The protein-tyrosine kinase oncogenes will be the primary focus of the review as discussed by the authors, however, biochemical connections between the protein tyrosine Kinases and oncoproteins of the Ras,Raf,Fos,Jun, and Rel families as well as the protein kinase C family are also discussed.
Journal ArticleDOI

Pathogenesis of NIDDM: A balanced overview

TL;DR: Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered β-cell function in NIDDM.
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The SH2 and SH3 domain-containing protein GRB2 links receptor tyrosine kinases to ras signaling

TL;DR: Results suggest that GRB2/sem-5 plays a crucial role in a highly conserved mechanism for growth factor control of ras signaling.
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Structure of the insulin receptor substrate IRS-1 defines a unique signal transduction protein.

TL;DR: During insulin stimulation, the IRS-1 protein undergoes tyrosine phosphorylation and binds phosphatidylinositol 3-kinase, suggesting that IRS–1 acts as a multisite Mocking' protein to bind signal-transducing molecules containing Src-homology 2 and SRC-Homology-3 domains, which may link the insulin receptor kinase and enzymes regulating cellular growth and metabolism.
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