Regulation of ERK1 and ERK2 by glucose and peptide hormones in pancreatic β cells

Don Arnette, Tara Beers Gibson, Michael C. Lawrence, Bridgette January, Shih Khoo, Kathleen McGlynn, Colleen A. Vanderbilt, Melanie H. Cobb

Research output: Contribution to journalArticlepeer-review

112 Scopus citations


We showed previously that ERK1/2 were activated by glucose and amino acids in pancreatic β cells. Here we examine and compare signaling events that are necessary for ERK1/2 activation by glucose and other stimuli in β cells. We find that agents that interrupt Ca2+ signaling by a variety of mechanisms interfere with glucose- and glucagon-like peptide (GLP-1)-stimulated ERK1/2 activity. In particular, calmodulin antagonists, FK506, and cyclosporin, immunosuppressants that inhibit the calcium-dependent phosphatase calcineurin, suppress ERK1/2 activation by both glucose and GLP-1. Ca2+ signaling from intracellular stores is also essential for ERK1/ 2 activation, because thapsigargin blocks ERK1/2 activation by glucose or GLP-1. The glucosesensitive mechanism is distinct from that used by phorbol ester or insulin to stimulate ERK1/2 but shares common features with that used by GLP-1.

Original languageEnglish (US)
Pages (from-to)32517-32525
Number of pages9
JournalJournal of Biological Chemistry
Issue number35
StatePublished - Aug 29 2003

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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