PMID: 7540574Jul 1, 1995Paper

Glucose-induced insulin receptor tyrosine phosphorylation in insulin-secreting beta-cells

Diabetes
P L RothenbergB A Wolf

Abstract

In the beta TC3 insulin-secreting beta-cell line, glucose rapidly induces the tyrosine phosphorylation of the 97-kDa insulin receptor beta-subunit. Phosphorylation is transient, with fourfold stimulation by 2 min and subsequent dephosphorylation to basal levels by 10-15 min. Elevating the extracellular KCl concentration equipotently initiates receptor phosphorylation. Preventing insulin secretion with 1 mumol/l epinephrine or by removing extracellular Ca2+ blocks the effect. In the absence of glucose-induced secretion, exogenous insulin also stimulated insulin receptor autophosphorylation transiently and with an ED50 of 4 x 10(-9) mol/l. In addition, functional insulin-like growth factor I (IGF-I) receptors are also expressed by these beta-cells, as indicated by IGF-I-induced receptor tyrosine phosphorylation (ED50 = 5 x 10(-9) mol/l) and also by detection of hybrid insulin/IGF-I receptor autophosphorylation at 10(-7) mol/l IGF-I. Both glucose and insulin stimulate the tyrosine phosphorylation of the insulin receptor substrate (IRS) IRS-1 and increase by two- to fivefold the rapid association of IRS-1 with the 85-kDa alpha-subunit of the phosphatidylinositol-3-kinase, as determined by co-immunoprecipitation assays. These result...Continue Reading

Citations

Jun 20, 2001·Acta Physiologica Scandinavica·C G Ostenson
May 17, 2008·Annual Review of Nutrition·Ingo B LeibigerPer-Olof Berggren
Aug 3, 1999·The Journal of Clinical Investigation·O PorzioG Sesti
Dec 22, 1999·The Journal of Clinical Investigation·R N KulkarniC R Kahn
Jun 16, 2011·International Journal of General Medicine·Olivia Mayasari TandrasasmitaRaymond Rubianto Tjandrawinata
Jul 24, 2013·Journal of the American Podiatric Medical Association·Maria Luz Gonzalez FernandezJuan Vicente Beneit Montesinos
May 1, 2007·Diabetes Research and Clinical Practice·Sung Hee-ParkDae-Kyu Song
Dec 23, 2014·Basic & Clinical Pharmacology & Toxicology·Anne Wuttke
Jul 21, 2016·PloS One·Elias N KatsoulierisEffie C Tsilibary
Apr 23, 1999·Journal of Basic and Clinical Physiology and Pharmacology·M E Patti, C R Kahn
Mar 11, 2020·International Journal of Molecular Sciences·Nadia Rachdaoui
Jul 6, 2001·International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity·E MuscelliM J Saad
Nov 26, 2002·Journal of Cellular Physiology·E P HaberA R Carpinelli
Feb 26, 1999·The Journal of Biological Chemistry·C A AspinwallR T Kennedy
Jun 5, 2003·FEBS Letters·Esther P HaberCarla R O Carvalho
Apr 18, 2003·International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity·J A PereiraE Muscelli
Jul 11, 2012·Journal of Receptor and Signal Transduction Research·Bożenna OleszczakMonika Pliszka
Feb 12, 1998·The Journal of Biological Chemistry·C A AspinwallJ R Lakey
Feb 24, 2001·Annals of the New York Academy of Sciences·K TrümperD Hörsch
Jan 14, 2003·The Journal of Biological Chemistry·Prabhakar D Borge, Bryan A Wolf
Nov 9, 2002·American Journal of Physiology. Endocrinology and Metabolism·Christopher J BarkerPer-Olof Berggren

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