NDLI: Lipid raft microdomain compartmentalization of TC10 is required for insulin signaling and GLUT4 translocation

Content Provider	PubMed Central
Author	Watson, Robert T. Shigematsu, Satoshi Chiang, Shian-huey Mora, Silvia Kanzaki, Makoto Macara, Ian G. Saltiel, Alan R. Pessin, Jeffrey E.
Abstract	Recent studies indicate that insulin stimulation of glucose transporter (GLUT)4 translocation requires at least two distinct insulin receptor–mediated signals: one leading to the activation of phosphatidylinositol 3 (PI-3) kinase and the other to the activation of the small GTP binding protein TC10. We now demonstrate that TC10 is processed through the secretory membrane trafficking system and localizes to caveolin-enriched lipid raft microdomains. Although insulin activated the wild-type TC10 protein and a TC10/H-Ras chimera that were targeted to lipid raft microdomains, it was unable to activate a TC10/K-Ras chimera that was directed to the nonlipid raft domains. Similarly, only the lipid raft–localized TC10/ H-Ras chimera inhibited GLUT4 translocation, whereas the TC10/K-Ras chimera showed no significant inhibitory activity. Furthermore, disruption of lipid raft microdomains by expression of a dominant-interfering caveolin 3 mutant (Cav3/DGV) inhibited the insulin stimulation of GLUT4 translocation and TC10 lipid raft localization and activation without affecting PI-3 kinase signaling. These data demonstrate that the insulin stimulation of GLUT4 translocation in adipocytes requires the spatial separation and distinct compartmentalization of the PI-3 kinase and TC10 signaling pathways.
Related Links	http://dx.doi.org/10.1083/jcb.200102078
Ending Page	840
Page Count	12
Starting Page	829
File Format	PDF
ISSN	00219525
e-ISSN	15408140
Journal	The Journal of Cell Biology
Issue Number	4
Volume Number	154
Language	English
Publisher	The Rockefeller University Press
Publisher Date	2001-08-20
Access Restriction	Open
Rights Holder	The Rockefeller University Press
Subject Keyword	Cell Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine

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