JBC Origene Your Gene Company

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on January 6, 2006
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow Supplemental Data
Right arrow All Versions of this Article:
281/1/484    most recent
M505944200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Martin, O. J.
Right arrow Articles by McGraw, T. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Martin, O. J.
Right arrow Articles by McGraw, T. E.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Papers In Press, published online ahead of print November 2, 2005
J. Biol. Chem, 10.1074/jbc.M505944200
Submitted on June 1, 2005
Accepted on November 2, 2005

GLUT4 distribution between the plasma membrane and the intracellular compartments is maintained by an insulin-modulated bipartite dynamic mechanism

Ola J. Martin, Adrian Lee, and Timothy E. McGraw

Biochemistry Dept., Weill Cornell Medical College, New York, NY 10021

Corresponding Author: temcgraw{at}med.cornell.edu

The GLUT4 glucose transporter is predominantly retained inside basal fat and muscle cells, and it is rapidly recruited to the plasma membrane with insulin stimulation. There is controversy regarding the mechanism of basal GLUT4 retention. One model is that GLUT4 retention is dynamic, based on slow exocytosis and rapid internalization of the entire pool of GLUT4 (Mol. Biol. Cell 15:870-882, 2004). In this model insulin increases GLUT4 in the plasma membrane by modulating GLUT4 exocytosis and endocytosis. The second model is that GLUT4 retention is static; with ~90% of GLUT4 stored in compartments that are not in equilibrium with the cell surface in basal conditions (Mol Cell Biol. 24:6456-6466, 2004). In this model insulin increases GLUT4 in the plasma membrane by releasing it from the static storage compartment. Here we show that under all experimental conditions examined, basal GLUT4 retention is by a bipartite dynamic mechanism involving slow efflux and rapid internalization. To establish that the dynamic model developed in studies of the extreme conditions of >100 nM insulin and no insulin, also describe GLUT4 behavior at more physiological insulin concentrations, we characterized GLUT4 trafficking in 0.5 nM insulin. This sub maximal insulin concentration promotes an intermediate effect on both GLUT4 exocytosis and endocytosis, resulting in an intermediate degree of redistribution to the plasma membrane. These data establish that changes in the steady-state surface-to-total distributions of GLUT4 are the result of gradated, insulin-induced changes in GLUT4 exocytosis and endocytosis rate.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Mol. Biol. CellHome page
V. Blot and T. E. McGraw
Molecular Mechanisms Controlling GLUT4 Intracellular Retention
Mol. Biol. Cell, August 1, 2008; 19(8): 3477 - 3487.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
X. M. Song, R. C. Hresko, and M. Mueckler
Identification of Amino Acid Residues within the C Terminus of the Glut4 Glucose Transporter That Are Essential for Insulin-stimulated Redistribution to the Plasma Membrane
J. Biol. Chem., May 2, 2008; 283(18): 12571 - 12585.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Endocrinol.Home page
M. Larance, G. Ramm, and D. E. James
The GLUT4 Code
Mol. Endocrinol., February 1, 2008; 22(2): 226 - 233.
[Abstract] [Full Text] [PDF]

Home page
 JCBHome page
D. Williams and J. E. Pessin
Mapping of R-SNARE function at distinct intracellular GLUT4 trafficking steps in adipocytes
J. Cell Biol., January 28, 2008; 180(2): 375 - 387.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
J. M. Muretta, I. Romenskaia, and C. C. Mastick
Insulin Releases Glut4 from Static Storage Compartments into Cycling Endosomes and Increases the Rate Constant for Glut4 Exocytosis
J. Biol. Chem., January 4, 2008; 283(1): 311 - 323.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C. A. Eyster, Q. S. Duggins, G. J. Gorbsky, and A. L. Olson
Microtubule Network Is Required for Insulin Signaling through Activation of Akt/Protein Kinase B: EVIDENCE THAT INSULIN STIMULATES VESICLE DOCKING/FUSION BUT NOT INTRACELLULAR MOBILITY
J. Biol. Chem., December 22, 2006; 281(51): 39719 - 39727.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Biol. CellHome page
E. Gonzalez and T. E. McGraw
Insulin Signaling Diverges into Akt-dependent and -independent Signals to Regulate the Recruitment/Docking and the Fusion of GLUT4 Vesicles to the Plasma Membrane
Mol. Biol. Cell, October 1, 2006; 17(10): 4484 - 4493.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2005 by the American Society for Biochemistry and Molecular Biology.