Reference : Phosphatidylinositol 3,4,5-trisphosphate modulation in Ship2-deficient mouse embryonic f...
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Life sciences : Genetics & genetic processes
http://hdl.handle.net/2268/32200
Phosphatidylinositol 3,4,5-trisphosphate modulation in Ship2-deficient mouse embryonic fibroblasts
English
Blero, D. [Université Libre de Bruxelles - ULB > Interdisciplinary Research Institute > > >]
Zhang, J. [Université Libre de Bruxelles - ULB > Interdisciplinary Research Institute (IRIBHM) > > >]
Pesesse, X. [Université Libre de Bruxelles - ULB > Interdisciplinary Research Institute (IRIBHM) > > >]
Payrastre, B. [INSERM U563 > , Departement d’Oncogenese et Signalization dans les Cellules Hematopoietiques, Hoˆ pital Purpan, Toulouse Cedex, France > > >]
Dumont, J. E. [Université Libre de Bruxelles - ULB > Interdisciplinary Research Institute (IRIBHM) > > >]
Schurmans, Stéphane mailto [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire > > >]
Erneux, C. [Université Libre de Bruxelles - ULB > Interdisciplinary Research Institute (IRIBHM) > > >]
2005
FEBS Journal
Blackwell Publishing
272
2512-2522
Yes (verified by ORBi)
International
1742-464X
Oxford
United Kingdom
[en] inositol 5-phosphatase ; mouse embryonic fibroblasts ; phosphatidylinositol 3,4,5-trisphosphate ; SH2 domain ; signal transduction
[en] SHIP2, the ubiquitous SH2 domain containing inositol 5-phosphatase, includes a series of protein interacting domains and has the ability to dephosphorylate phosphatidylinositol 3,4,5-trisphosphate [PtdIns(3,4,5)P3] in vitro. The present study, which was undertaken to evaluate the impact of SHIP2 on PtdIns(3,4,5)P3 levels, was performed in a mouse embryonic fibroblast (MEF) model using SHIP2 deficient (– ⁄ –) MEF cells derived from knockout mice. PtdIns(3,4,5)P3 was upregulated in serum stimulated – ⁄ – MEF cells as compared to +⁄+ MEF cells. Although the absence of SHIP2 had no effect on basal PtdIns(3,4,5)P3 levels, we show here that this lipid was significantly upregulated in SHIP2 – ⁄ – cells but only after short-term (i.e. 5–10 min) incubation with serum. The difference in PtdIns(3,4,5)P3 levels in heterozygous fibroblast cells was intermediate between the +⁄+ and the – ⁄ – cells. In our model, insulin-like growth factor-1 stimulation did not show this upregulation. Serum stimulated phosphoinositide 3-kinase (PI 3-kinase) activity appeared to be comparable between +⁄+ and – ⁄ – cells. Moreover, protein kinase B, but not mitogen activated protein kinase activity, was also potentiated in SHIP2 deficient cells stimulated by serum. The upregulation of protein kinase B activity in serum stimulated cells was totally reversed in the presence of the PI 3-kinase inhibitor LY-294002, in both +⁄+ and – ⁄ – cells. Altogether, these data establish a link between SHIP2 and the acute control of PtdIns(3,4,5)P3 levels in intact cells
Researchers ; Professionals
http://hdl.handle.net/2268/32200
Abbreviations: CHO-IR, chinese hamster ovary cells overexpressing the insulin receptor; EGF, epidermal growth factor; FBS, foetal bovine serum; FGF, fibroblast growth factor; HGF, hepatocyte growth factor; IGF, insulin-like growth factor; MAP, mitogen activated protein; M-CSF, macrophage colony-stimulating factor; MEF, mouse embryonic fibroblast; PDGF, platelet-derived growth factor; PI 3-kinase, phosphoinositide 3-kinase; PKB, protein kinase B; PtdIns(3,4)P2, phosphatidylinositol 3,4-bisphosphate; PtdIns(3,4,5)P3, phosphatidylinositol 3,4,5-trisphosphate; PtdIns4P, phosphatidylinositol 4-phosphate; PtdIns(4,5)P2, phosphatidylinositol 4,5-bisphosphate; PTEN, phosphate and tension homolog deleted on chromosome 10; SHIP, SH2 domain containing inositol phosphatase

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