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
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