J
Jerrold M. Olefsky
Researcher at University of California, San Diego
Publications - 606
Citations - 83310
Jerrold M. Olefsky is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Insulin & Insulin resistance. The author has an hindex of 143, co-authored 595 publications receiving 77356 citations. Previous affiliations of Jerrold M. Olefsky include University of Colorado Boulder & University of Michigan.
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Journal ArticleDOI
The signaling pathway coupling epidermal growth factor receptors to activation of p21ras.
TL;DR: Data indicate that coupling to Shc provides the major pathway linking activated EGFRs to Grb2.Sos and stimulation of the p21ras pathway.
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Inhibition of Phosphatidylinositol 3-Kinase Activity by Adenovirus-mediated Gene Transfer and Its Effect on Insulin Action
Prem M. Sharma,Katsuya Egawa,Yi Huang,Jody L. Martin,Ivana Huvar,Gerry R. Boss,Jerrold M. Olefsky +6 more
TL;DR: It is concluded that, in 3T3-L1 adipocytes, non-IRS-1-associated PI 3-kinase activity is crucial for insulin’s metabolic signaling, and that overexpressed p85N-SH2 protein inhibits a variety of insulin's ultimate biological effects.
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Insulin receptor substrate 1 is required for insulin-mediated mitogenic signal transduction.
TL;DR: Microinjection of anti-IRS-1 antibody completely inhibited incorporation of bromodeoxyuridine into the nuclei of cells stimulated with insulin or insulin-like growth factor I but did not affect cells stimulating with serum or a variety of purified growth factors.
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Role of Glucose Transport in the Postreceptor Defect of Non-insulin-dependent Diabetes Mellitus
TL;DR: The insulin resistance in subjects with IGT is due solely to a decrease in insulin binding, whereas subjects with NIDDM exhibit both decreased insulin binding and decreased maximal rates of insulin-stimulated adipocyte glucose transport due to a postreceptor defect at this site in the insulin action pathway.
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Effect of Troglitazone on Leptin Production: Studies In Vitro and in Human Subjects
TL;DR: It appears that obese subjects are resistant to the effects of endogenously secreted leptin, as there was no significant change in fasting plasma leptin concentrations, despite a 40–50% reduction in fasting and postmeal plasma insulin concentrations.