Abstract
Insulin stimulates the delivery of glucose transporter-4 (GLUT4)-containing vesicles to the surface of adipocytes. Depletion of the Sec1/Munc18 protein mVps45 significantly abrogates insulin-stimulated glucose transport and GLUT4 translocation. Here we show that depletion of mVps45 selectively reduced expression of VAMPs 2 and 4, but not other VAMP isoforms. Although we did not observe direct interaction of mVps45 with any VAMP isoform; we found that the cognate binding partner of mVps45, Syntaxin 16 associates with VAMPs 2, 4, 7 and 8 in vitro. Co-immunoprecipitation experiments in 3T3-L1 adipocytes revealed an interaction between Syntaxin 16 and only VAMP4. We suggest GLUT4 trafficking is controlled by the coordinated expression of mVps45/Syntaxin 16/VAMP4, and that depletion of mVps45 regulates VAMP2 levels indirectly, perhaps via reduced trafficking into specialized subcellular compartments.
| Original language | English |
|---|---|
| Pages (from-to) | 1-5 |
| Number of pages | 5 |
| Journal | Communicative & integrative biology |
| Volume | 8 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 24 Jun 2015 |
Keywords
- Adipocyte
- Biochemistry
- Cell biology
- Glucose transport
- Hormones
- Insulin
- Intracellular membranes
- Membrane protein trafficking
- Membrane trafficking
- SNARE proteins
- VAMP