SHIP2 controls PtdIns(3,4,5)P3 levels and PKB activity inresponse to oxidative stress

Zhang Jing, Zhenan Liu, Joanne Rasschaert, Daniel Blero, Laurence Deneubourg, Stéphane Schurmans, Christophe Erneux, Xavier Pesesse

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Abstract
Reactive oxygen species (ROS) are known to be involved in redox signalling pathways that may contribute to normal cell function as well as
disease progression. The tumour suppressor PTEN and the inositol 5-phosphatase SHIP2 are critical enzymes in the control of PtdIns(3,4,5)P3
level. It has been reported that oxidants, including those produced in cells such as macrophages, can activate downstream signalling via the
inactivation of PTEN. The present study evaluates the potential impact of SHIP2 on phosphoinositides in cells exposed to sodium peroxide. We
used a model of SHIP2 deficient mouse embryonic fibroblasts (MEFs) stimulated by H2O2: at 15 min, PtdIns(3,4,5)P3 was markedly increased in
SHIP2 ?/? cells as compared to +/+ cells. In contrast, no significant increase in PtdIns(3,4)P2 could be detected at 15 or 120 min incubation of the
cells with H2O2 (0.6 mM). PKB activity was also upregulated in SHIP2 ?/? cells as compared to +/+ cells in response to H2O2. SHIP2 add back
experiments in SHIP2 ?/? cells confirm its critical role as a lipid phosphatase in the control of PtdIns(3,4,5)P3 level in response to H2O2. We
conclude that SHIP2 lipid phosphatase activity plays an important role in the metabolism PtdIns(3,4,5)P3 which is demonstrated in oxygen
stressed cells.
Original languageEnglish
Pages (from-to)2194-2200
Number of pages6
JournalCellular Signalling
Volume19
Issue number10
Publication statusPublished - Oct 2007

Keywords

  • SHIP2
  • Inositol 5-phosphatase;
  • Mouse embryonic fibroblasts

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