Regulation of phosphatidylinositol 3,4,5-trisphosphate 5'-phosphatase activity by insulin
- PMID: 8939879
- DOI: 10.1074/jbc.271.47.29533
Regulation of phosphatidylinositol 3,4,5-trisphosphate 5'-phosphatase activity by insulin
Abstract
Polyphosphoinositides are thought to be mediators of cellular signaling pathways as well as regulators of cytoskeletal elements and membrane trafficking events. It has recently been demonstrated that a class of phosphatidylinositol (PI) 3,4,5-P3 5'-phosphatases contains SH2 domains and proline-rich regions, which are present in many signaling proteins. We report here that insulin stimulation of Chinese hamster ovary cells (CHO-T) expressing human insulin receptors causes an 8-10-fold increase in PI 3,4,5-P3 5'-phosphatase activity in anti-phosphotyrosine immunoprecipitates of the cell lysates. This insulin-sensitive polyphosphoinositide 5'-phosphatase did not catalyze dephosphorylation of PI 4,5-P2. No change in 5'-phosphatase activity was detected in insulin receptor or IRS-1 immune complexes in response to insulin. However, insulin treatment of CHO-T cells markedly increased the PI 3,4,5-P3 5'-phosphatase activity associated with Shc and Grb2. The insulin-regulated polyphosphoinositide 5'-phosphatase was not immunoreactive with antibody raised against the recently cloned SHIP 5'-phosphatase reported to associate with Shc and Grb2 in B lymphocytes. These data demonstrate that insulin causes formation of complexes containing a PI 3,4,5-P3 5'-phosphatase, and Shc or Grb2, or both, suggesting an important role of this enzyme in insulin signaling.
Similar articles
-
Overexpression of SH2-containing inositol phosphatase 2 results in negative regulation of insulin-induced metabolic actions in 3T3-L1 adipocytes via its 5'-phosphatase catalytic activity.Mol Cell Biol. 2001 Mar;21(5):1633-46. doi: 10.1128/MCB.21.5.1633-1646.2001. Mol Cell Biol. 2001. PMID: 11238900 Free PMC article.
-
Molecular cloning of rat SH2-containing inositol phosphatase 2 (SHIP2) and its role in the regulation of insulin signaling.Biochem Biophys Res Commun. 1999 Jun 24;260(1):265-72. doi: 10.1006/bbrc.1999.0888. Biochem Biophys Res Commun. 1999. PMID: 10381377
-
Mechanism of SHIP-mediated inhibition of insulin- and platelet-derived growth factor-stimulated mitogen-activated protein kinase activity in 3T3-L1 adipocytes.Mol Endocrinol. 2005 Feb;19(2):421-30. doi: 10.1210/me.2004-0096. Epub 2004 Oct 14. Mol Endocrinol. 2005. PMID: 15486046
-
The SH2 domain containing inositol 5-phosphatase SHIP2 controls phosphatidylinositol 3,4,5-trisphosphate levels in CHO-IR cells stimulated by insulin.Biochem Biophys Res Commun. 2001 Apr 6;282(3):839-43. doi: 10.1006/bbrc.2001.4639. Biochem Biophys Res Commun. 2001. PMID: 11401540
-
SHIP, a new player in cytokine-induced signalling.Leukemia. 1997 Feb;11(2):181-4. doi: 10.1038/sj.leu.2400559. Leukemia. 1997. PMID: 9009077 Review.
Cited by
-
A high-avidity biosensor reveals plasma membrane PI(3,4)P2 is predominantly a class I PI3K signaling product.J Cell Biol. 2019 Mar 4;218(3):1066-1079. doi: 10.1083/jcb.201809026. Epub 2018 Dec 27. J Cell Biol. 2019. PMID: 30591513 Free PMC article.
-
AKT/PKB Signaling: Navigating the Network.Cell. 2017 Apr 20;169(3):381-405. doi: 10.1016/j.cell.2017.04.001. Cell. 2017. PMID: 28431241 Free PMC article. Review.
-
Overexpression of SH2-containing inositol phosphatase 2 results in negative regulation of insulin-induced metabolic actions in 3T3-L1 adipocytes via its 5'-phosphatase catalytic activity.Mol Cell Biol. 2001 Mar;21(5):1633-46. doi: 10.1128/MCB.21.5.1633-1646.2001. Mol Cell Biol. 2001. PMID: 11238900 Free PMC article.
-
Ceramide dissociates 3'-phosphoinositide production from pleckstrin homology domain translocation.Biochem J. 2001 Mar 1;354(Pt 2):359-68. doi: 10.1042/0264-6021:3540359. Biochem J. 2001. PMID: 11171115 Free PMC article.
-
Confocal imaging of the subcellular distribution of phosphatidylinositol 3,4,5-trisphosphate in insulin- and PDGF-stimulated 3T3-L1 adipocytes.Biochem J. 1999 Dec 1;344 Pt 2(Pt 2):511-8. Biochem J. 1999. PMID: 10567235 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical
Research Materials
Miscellaneous