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Coordination of cell signaling and transport machinery during insulin-stimulated glucose transport
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ISBN 9780549510017
REGISTERED: 11/18/17
UPDATED: 10/21/19
Coordination of cell signaling and transport machinery during insulin-stimulated glucose transport.
Insulin-stimulated glucose transport is the rate-limiting step in glucose disposal and utilization. Insulin increases glucose uptake in fat and muscle through the translocation of the insulin-responsive glucose transporter GI ut4 to the plasma membrane. Although our understanding of the pathways governing this process remain incomplete, small GTPases have been implicated as "molecular switches" that operate at the crossroads of insulin signaling and Glut4 translocation. This thesis


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  • ISBN bar code 9780549510017 ξ1 registered March 17 2016
  • Product category is Coordination-of-cell-signaling-and-transport-machinery-during-insulin-stimulated-glucose-transport Xiao-wei-Chen Book

Insulin-stimulated glucose transport is the rate-limiting step in glucose disposal and utilization. Insulin increases glucose uptake in fat and muscle through the translocation of the insulin-responsive glucose transporter GI ut4 to the plasma membrane. Although our understanding of the pathways governing this process remain incomplete, small GTPases have been implicated as "molecular switches" that operate at the crossroads of insulin signaling and Glut4 translocation. This thesis elucidates the role of RalA, a small GTPase that regulates an octameric vesicle-tethering complex known as the exocyst during Glut4 trafficking. Initial studies on the cell cycle revealed that both RalA and the exocyst are involved in trafficking through the recycling endosome. Loss of RalA or the exocyst led to a specific blockade in cell abscission, the very last stage of cytokinesis, implying the involvement of these proteins in a subset of transport events under tight regulation. Glut4 traffics through the recycling endosome in adipocytes. We found that RA1A resides on the Glut4 vesicles and interacts with the exocyst in insulin-responsive cells. Insulin activates RA1A in a PI-3 kinase-dependent manner. Disruption of RalA function led to inhibition of insulin-stimulated glucose transport, as did loss of the exocyst. Furthermore, RalA also binds to Myo1c, a molecular motor previously implicated in Glut4 trafficking. This interaction is modulated by Calmodulin, which functions as the light chain for Myo1c during insulin-stimulated glucose transport. The data suggested a dual role for RA1A in insulin action, as a cargo receptor for Myo1c and a signal to unify the exocyst. The architecture of the exocyst complex was further dissected with RA1A mutants uncoupled from one branch of its effectors, including the two exocyst subunits Sec5 and Exo84. We found that both subunits are required for exocyst function in glucose transport; however, they belong to different branches of the


References
    ^ Coordination of cell signaling and transport machinery during insulin-stimulated glucose transport. (revised Oct 2019)

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