• Title of article

    SHIP, SHIP2, and PTEN activities are regulated in vivo by modulation of their protein levels: SHIP is up-regulated in macrophages and mast cells by lipopolysaccharide

  • Author/Authors

    Laura M. Sly، نويسنده , , Michael J. Rauh، نويسنده , , Janet Kalesnikoff، نويسنده , , Tom Büchse، نويسنده , , Gerald Krystal، نويسنده ,

  • Issue Information
    روزنامه با شماره پیاپی سال 2003
  • Pages
    12
  • From page
    1170
  • To page
    1181
  • Abstract
    The phosphatidylinositol-3 kinase (PI3K) pathway plays a central role in regulating numerous biologic processes, including survival, adhesion, migration, metabolic activity, proliferation, differentiation, and end cell activation through the generation of the potent second messenger PI-3,4,5-trisphosphate (PI-3,4,5-P3). To ensure that activation of this pathway is appropriately suppressed/terminated, the ubiquitously expressed 54-kDa tumor suppressor PTEN hydrolyzes PI-3,4,5-P3 to PI-4,5-P2, whereas the 145-kDa hematopoietic-restricted SH2-containing inositol 5′-phosphatase SHIP (also known as SHIP1), the 104-kDa stem cell-restricted SHIP sSHIP, and the more widely expressed 150-kDa SHIP2 break it down to PI-3,4-P2. In this review, we focus on the properties of these phospholipid phosphatases and summarize recent data showing that the activities of these negative regulators often are modulated by simply altering their protein levels. We also highlight the critical role that SHIP plays in lipopolysaccharide-induced macrophage activation and in endotoxin tolerance.
  • Journal title
    Experimental Hematology
  • Serial Year
    2003
  • Journal title
    Experimental Hematology
  • Record number

    513935