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Inhibition of SH2-domain containing inositol phosphatase 2 (SHIP2) in insulin producing INS1E cells improves insulin signal transduction and induces proliferation
Authors:Grempler Rolf  Leicht Stefanie  Kischel Ivonne  Eickelmann Peter  Redemann Norbert
Affiliation:Department of Metabolic Diseases Research, Boehringer Ingelheim Pharma GmbH & Co. KG, Birkendorfer Strasse 65, D-88397 Biberach an der Riss, Germany. rolfgrempler@yahoo.de
Abstract:Inhibition of the lipid phosphatase SH2-domain containing inositol phosphatase 2 (SHIP2) in L6-C10 muscle cells, in 3T3-L1 adipocytes and in the liver of db/db mice has been shown to ameliorate insulin signal transduction and established SHIP2 as a negative regulator of insulin action. Here we show that SHIP2 inhibition in INS1E insulinoma cells increased Akt, glycogen synthase kinase 3 and extracellular signal-regulated kinases 1 and 2 phosphorylation. SHIP2 inhibition did not prevent palmitate-induced apoptosis, but increased cell proliferation. Our data raise the interesting possibility that SHIP2 inhibition exerts proliferative effects in beta-cells and further support the attractiveness of a specific inhibition of SHIP2 for the treatment of type 2 diabetes.
Keywords:βGal, beta-galactosidase   ERK1/2, extracellular signal-regulated kinases 1 and 2   GLP-1, glucagon-like peptide 1   GSK3, glycogen synthase kinase 3   PI3K, phosphatidylinositol 3-kinase   PKB (Akt), protein kinase B   PtdIns(3,4,5)P3, phosphatidylinositol 3,4,5-trisphosphate   SHIP2, SH2-domain containing inositol phosphatase 2
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