Insulin Stimulates Actin Comet Tails on Intracellular GLUT4-containing Compartments in Differentiated 3T3L1 Adipocytes

Makoto Kanzaki, Robert T. Watson, Ahmir H. Khan, Jeffrey E. Pessin

研究成果: Article査読

71 被引用数 (Scopus)

抄録

Incubation of isolated GLUT4-containing vesicles with Xenopus oocyte extracts resulted in a guanosine 5′-[γ-thio]triphosphate (GTPγS) and sodium orthovanadate stimulation of actin comet tails. The in vitro actin-based GLUT4 vesicle motility was inhibited by both latrunculin B and a dominant-interfering N-WASP mutant, N-WASP/ΔVCA. Preparations of gently sheared (broken) 3T3L1 adipocytes also displayed GTPγS and sodium orthovanadate stimulation of actin comet tails on GLUT4 intracellular compartments. Furthermore, insulin pretreatment of intact adipocytes prior to gently shearing also resulted in a marked increase in actin polymerization and actin comet tailing on GLUT4 vesicles. In addition, the insulin stimulation of actin comet tails was completely inhibited by Clostridum difficile toxin B, demonstrating a specific role for a Rho family member small GTP-binding protein. Expression of N-WASP/ΔVCA in intact cells had little effect on adipocyte cortical actin but partially inhibited insulin-stimulated GLUT4 translocation. Taken together, these data demonstrate that insulin can induce GLUT4 vesicle actin comet tails that are necessary for the efficient translocation of GLUT4 from intracellular storage sites to the plasma membrane.

本文言語English
ページ(範囲)49331-49336
ページ数6
ジャーナルJournal of Biological Chemistry
276
52
DOI
出版ステータスPublished - 2001 12 28
外部発表はい

ASJC Scopus subject areas

  • 生化学
  • 分子生物学
  • 細胞生物学

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