Journal
BIOCHEMICAL JOURNAL
Volume 422, Issue -, Pages 229-235Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BJ20090624
Keywords
adipocytes; fluorescence resonance energy transfer (FRET); guanine-nucleotide-dissociation inhibitor (GDI); glucose transporter 4 (GLUT4); Rab10; total internal reflection microscopy (TIRFM)
Categories
Funding
- National Science Foundation of China [30630020]
- National Basic Research Program of China [2004CB720000]
- CAS Project [KSCX1-YW-02-01]
- Beijing Natural Science Foundation [5092017]
Ask authors/readers for more resources
Insulin stimulates GLUT4 (glucose transporter 4) translocation in adipocytes and muscles. An emerging picture is that Rab10 could bridge the gap between the insulin signalling cascade and GLUT4 translocation in adipocytes. In the present study, two potential effectors of Rab10, GDI (guanine-nucleotide-dissociation inhibitor)-1 and GDI-2, are characterized in respect to their roles in insulin-stimulated GLUT4 translocation. It is shown that both GDI-1 and GDI-2 exhibit similar distribution to GLUT4 and Rab10 at the TGN (trans-Golgi network) and periphery structures. Meanwhile, GDI-1 clearly interacts with Rab10 with higher affinity, as shown by both immunoprecipitation and in vivo FRET (fluorescence resonance energy transfer). In addition, the participation of GDIs in GLUT4 translocation is illustrated when overexpression of either GDI inhibits insulin-stimulated GLUT4 translocation in 3T3-L1 adipocytes. Taken together, we propose that GDI-1 is preferentially involved in insulin-stimulated GLUT4 translocation through facilitating Rab10 recycling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available