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The protein tyrosine phosphatase alpha modifies insulin secretion in INS-1E cells.

Authors
  • Kapp, Katja
  • Metzinger, Elisabeth
  • Kellerer, Monika
  • Häring, Hans-Ulrich
  • Lammers, Reiner
Type
Published Article
Journal
Biochemical and biophysical research communications
Publication Date
Nov 14, 2003
Volume
311
Issue
2
Pages
361–364
Identifiers
PMID: 14592422
Source
Medline
License
Unknown

Abstract

Increasing evidence indicates a role of insulin signalling for insulin secretion from the pancreatic beta-cells. Therefore, regulators of insulin signalling, like protein tyrosine phosphatases, could also have an impact on insulin secretion. Here, we investigated a possible role of the negative regulator protein tyrosine phosphatase alpha (PTP alpha) for insulin secretion. RT-PCR analysis confirmed that both splice variants of the extracellular domain of PTP alpha that vary by an insert of 9 amino acids are expressed in human islets and insulinoma cells (INS-1E, RIN1046-38). Overexpression of the wild type PTP alpha splice variant containing the 9 amino acids reduced insulin secretion, as did a mutant form unable to bind Grb2 (Tyr798Phe). By contrast, overexpression of a phosphatase inactive mutant improved insulin secretion. These data reveal a functional relevance of PTP alpha for insulin secretion.

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