![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 14, Issue 7, 2946-2958, July 2003
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
* The Henry Wellcome Laboratory of Cell Biology, Division of Biochemistry and
Molecular Biology, Institute of Biomedical and Life Sciences, University of
Glasgow, Glasgow G12 8QQ, Scotland;
School of Biochemistry and Genetics, The Medical School, University of
Newcastle, Newcastle-upon-Tyne NE2 4HH, United Kingdom; and
Institute of Molecular and Cell Biology, Singapore 117609, Republic of
Singapore
Submitted November 12, 2002;
Revised February 19, 2003;
Accepted March 10, 2003
Monitoring Editor: Suzanne Pfeffer
Insulin stimulates the movement of glucose transporter-4 (Glut4)–containing vesicles to the plasma membrane of adipose cells. We investigated the role of post-Golgi t-soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) in the trafficking of Glut4 in 3T3-L1 adipocytes. Greater than 85% of syntaxin 6 was found in Glut4-containing vesicles, and this t-SNARE exhibited insulin-stimulated movement to the plasma membrane. In contrast, the colocalization of Glut4 with syntaxin 7, 8, or 12/13 was limited and these molecules did not translocate to the plasma membrane. We used adenovirus to overexpress the cytosolic domain of these syntaxin's and studied their effects on Glut4 traffic. Overexpression of the cytosolic domain of syntaxin 6 did not affect insulin-stimulated glucose transport, but increased basal deGlc transport and cell surface Glut4 levels. Moreover, the syntaxin 6 cytosolic domain significantly reduced the rate of Glut4 reinternalization after insulin withdrawal and perturbed subendosomal Glut4 sorting; the corresponding domains of syntaxins 8 and 12 were without effect. Our data suggest that syntaxin 6 is involved in a membrane-trafficking step that sequesters Glut4 away from traffic destined for the plasma membrane. We speculate that this is at the level of traffic of Glut4 into its unique storage compartment and that syntaxin 16 may be involved.
Corresponding author. E-mail address:
g.gould{at}bio.gla.ac.uk.
This article has been cited by other articles:
|
|
 |
|
  R. T. Watson and J. E. Pessin Recycling of IRAP from the plasma membrane back to the insulin-responsive compartment requires the Q-SNARE syntaxin 6 but not the GGA clathrin adaptors J. Cell Sci., April 15, 2008; 121(8): 1243 - 1251. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 L. Nyasae, R. Bustos, L. Braiterman, B. Eipper, and A. Hubbard Dynamics of endogenous ATP7A (Menkes protein) in intestinal epithelial cells: copper-dependent redistribution between two intracellular sites Am J Physiol Gastrointest Liver Physiol, April 1, 2007; 292(4): G1181 - G1194. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Yu, J. Cresswell, M. G. Loffler, and J. S. Bogan The Glucose Transporter 4-regulating Protein TUG Is Essential for Highly Insulin-responsive Glucose Uptake in 3T3-L1 Adipocytes J. Biol. Chem., March 9, 2007; 282(10): 7710 - 7722. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Williams, S. W. Hicks, C. E. Machamer, and J. E. Pessin Golgin-160 Is Required for the Golgi Membrane Sorting of the Insulin-responsive Glucose Transporter GLUT4 in Adipocytes Mol. Biol. Cell, December 1, 2006; 17(12): 5346 - 5355. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. R. Peck, S. Ye, V. Pham, R. N. Fernando, S. L. Macaulay, S. Y. Chai, and A. L. Albiston Interaction of the Akt Substrate, AS160, with the Glucose Transporter 4 Vesicle Marker Protein, Insulin-Regulated Aminopeptidase Mol. Endocrinol., October 1, 2006; 20(10): 2576 - 2583. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Bose, A. Guilherme, S. Huang, A. C. Hubbard, C. R. Lane, N. A. Soriano, and M. P. Czech The v-SNARE Vti1a Regulates Insulin-stimulated Glucose Transport and Acrp30 Secretion in 3T3-L1 Adipocytes J. Biol. Chem., November 4, 2005; 280(44): 36946 - 36951. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Guo, L. Nyasae, L. T. Braiterman, and A. L. Hubbard NH2-terminal signals in ATP7B Cu-ATPase mediate its Cu-dependent anterograde traffic in polarized hepatic cells Am J Physiol Gastrointest Liver Physiol, November 1, 2005; 289(5): G904 - G916. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. S. L. Thong, C. B. Dugani, and A. Klip Turning Signals On and Off: GLUT4 Traffic in the Insulin-Signaling Highway Physiology, August 1, 2005; 20(4): 271 - 284. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Nakamura, H. Fukuda, A. Kato, and S. Hirose MARCH-II Is a Syntaxin-6-binding Protein Involved in Endosomal Trafficking Mol. Biol. Cell, April 1, 2005; 16(4): 1696 - 1710. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Guilherme, N. A. Soriano, P. S. Furcinitti, and M. P. Czech Role of EHD1 and EHBP1 in Perinuclear Sorting and Insulin-regulated GLUT4 Recycling in 3T3-L1 Adipocytes J. Biol. Chem., September 17, 2004; 279(38): 40062 - 40075. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. A. Bauer, R. L. Overlease, J. L. Lieber, and J. K. Angleson Retention and stimulus-dependent recycling of dense core vesicle content in neuroendocrine cells J. Cell Sci., May 1, 2004; 117(11): 2193 - 2202. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Karylowski, A. Zeigerer, A. Cohen, and T. E. McGraw GLUT4 Is Retained by an Intracellular Cycle of Vesicle Formation and Fusion with Endosomes Mol. Biol. Cell, February 1, 2004; 15(2): 870 - 882. [Abstract] [Full Text] [PDF]
|
|
