mVps45 knockdown selectively modulates VAMP expression in 3T3-L1 adipocytes

Research output: Contribution to journalArticle

Published copy (DOI)

Author(s)

  • Jessica B A Sadler
  • Jennifer Roccisana
  • Minttu Virolainen
  • Nia J. Bryant
  • Gwyn W. Gould

Department/unit(s)

Publication details

JournalCommunicative & integrative biology
DatePublished - 24 Jun 2015
Issue number3
Volume8
Number of pages5
Pages (from-to)1-5
Original languageEnglish

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.

    Research areas

  • Adipocyte, Biochemistry, Cell biology, Glucose transport, Hormones, Insulin, Intracellular membranes, Membrane protein trafficking, Membrane trafficking, SNARE proteins, VAMP

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