Insulin signaling: GLUT4 vesicles exit via the exocyst

Makoto Kanzaki; Jeffrey E. Pessin

doi:10.1016/S0960-9822(03)00478-0

Insulin signaling: GLUT4 vesicles exit via the exocyst

Makoto Kanzaki, Jeffrey E. Pessin

MEN - Biomedical Engineering

Stony Brook University

Research output: Contribution to journal › Review article › peer-review

54 Citations (Scopus)

Abstract

The localization of the GTP-binding protein TC10 to lipid raft microdomains has been suggested to play a role in the stimulation of GLUT4 translocation. The exocyst has now been identified as a downstream target for TC10, directing GLUT4-containing vesicles to the site of fusion.

Original language	English
Pages (from-to)	R574-R576
Journal	Current Biology
Volume	13
Issue number	14
DOIs	https://doi.org/10.1016/S0960-9822(03)00478-0
Publication status	Published - 2003 Jul 15

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title = "Insulin signaling: GLUT4 vesicles exit via the exocyst",

abstract = "The localization of the GTP-binding protein TC10 to lipid raft microdomains has been suggested to play a role in the stimulation of GLUT4 translocation. The exocyst has now been identified as a downstream target for TC10, directing GLUT4-containing vesicles to the site of fusion.",

author = "Makoto Kanzaki and Pessin, {Jeffrey E.}",

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AU - Kanzaki, Makoto

AU - Pessin, Jeffrey E.

PY - 2003/7/15

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N2 - The localization of the GTP-binding protein TC10 to lipid raft microdomains has been suggested to play a role in the stimulation of GLUT4 translocation. The exocyst has now been identified as a downstream target for TC10, directing GLUT4-containing vesicles to the site of fusion.

AB - The localization of the GTP-binding protein TC10 to lipid raft microdomains has been suggested to play a role in the stimulation of GLUT4 translocation. The exocyst has now been identified as a downstream target for TC10, directing GLUT4-containing vesicles to the site of fusion.

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SN - 0960-9822

VL - 13

SP - R574-R576

JO - Current Biology

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Insulin signaling: GLUT4 vesicles exit via the exocyst

Abstract

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