Inhibition of GLUT4 translocation by Tbc1d1, a Rab GTPase-activating protein abundant in skeletal muscle, is partially relieved by AMP-activated protein kinase activation.
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Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscleMuscle cells engage Rab8A and myosin Vb in insulin-dependent GLUT4 translocationDisruption of AMPKalpha1 signaling prevents AICAR-induced inhibition of AS160/TBC1D4 phosphorylation and glucose uptake in primary rat adipocytesGenetic disruption of AMPK signaling abolishes both contraction- and insulin-stimulated TBC1D1 phosphorylation and 14-3-3 binding in mouse skeletal muscleInsulin-stimulated phosphorylation of the Rab GTPase-activating protein TBC1D1 regulates GLUT4 translocationRab GAPs AS160 and Tbc1d1 play nonredundant roles in the regulation of glucose and energy homeostasis in miceDeletion of the Rab GAP Tbc1d1 modifies glucose, lipid, and energy homeostasis in miceDisruption of Adipose Rab10-Dependent Insulin Signaling Causes Hepatic Insulin Resistance.Exercise and type 2 diabetes: molecular mechanisms regulating glucose uptake in skeletal muscle.Deletion of Rab GAP AS160 modifies glucose uptake and GLUT4 translocation in primary skeletal muscles and adipocytes and impairs glucose homeostasis.Regulation of glucose transporter 4 translocation by the Rab guanosine triphosphatase-activating protein AS160/TBC1D4: role of phosphorylation and membrane association.Identification of a novel phosphorylation site on TBC1D4 regulated by AMP-activated protein kinase in skeletal muscleSpatiotemporal Regulators for Insulin-Stimulated GLUT4 Vesicle Exocytosis.TBC1D1 regulates insulin- and contraction-induced glucose transport in mouse skeletal muscle.Leptin reduces the expression and increases the phosphorylation of the negative regulators of GLUT4 traffic TBC1D1 and TBC1D4 in muscle of ob/ob mice.A role for AMPK in increased insulin action after serum starvationThe integration of autophagy and cellular trafficking pathways via RAB GAPsRapid reversal of insulin-stimulated AS160 phosphorylation in rat skeletal muscle after insulin exposureDeficiency in AMP-activated protein kinase exaggerates high fat diet-induced cardiac hypertrophy and contractile dysfunctionSignaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis.Roles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscleEmerging role for AS160/TBC1D4 and TBC1D1 in the regulation of GLUT4 trafficMice with AS160/TBC1D4-Thr649Ala knockin mutation are glucose intolerant with reduced insulin sensitivity and altered GLUT4 trafficking.Clustering of GLUT4, TUG, and RUVBL2 protein levels correlate with myosin heavy chain isoform pattern in skeletal muscles, but AS160 and TBC1D1 levels do notInsulin and AMPK regulate FA translocase/CD36 plasma membrane recruitment in cardiomyocytes via Rab GAP AS160 and Rab8a Rab GTPaseRegulatory mode shift of Tbc1d1 is required for acquisition of insulin-responsive GLUT4-trafficking activity.Potential role of TBC1D4 in enhanced post-exercise insulin action in human skeletal muscle.Contraction-stimulated glucose transport in rat skeletal muscle is sustained despite reversal of increased PAS-phosphorylation of AS160 and TBC1D1Reduced activity of AMP-activated protein kinase protects against genetic models of motor neuron disease.Inhibition of contraction-stimulated AMP-activated protein kinase inhibits contraction-stimulated increases in PAS-TBC1D1 and glucose transport without altering PAS-AS160 in rat skeletal muscle.Acute resistance exercise-induced IGF1 expression and subsequent GLUT4 translocation.Increased AS160 phosphorylation, but not TBC1D1 phosphorylation, with increased postexercise insulin sensitivity in rat skeletal muscle.A common trafficking route for GLUT4 in cardiomyocytes in response to insulin, contraction and energy-status signallingAMP-activated protein kinase promotes human prostate cancer cell growth and survival.Exercise and insulin: Convergence or divergence at AS160 and TBC1D1?SNARE proteins underpin insulin-regulated GLUT4 traffic.Inhibition and termination of physiological responses by GTPase activating proteins.AMP-activated protein kinase regulation and biological actions in the heart.AMP-activated protein kinase activators in diabetic ulcers: from animal studies to Phase II drugs under investigation.Role of Rab GTPases and their interacting proteins in mediating metabolic signalling and regulation.
P2860
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P2860
Inhibition of GLUT4 translocation by Tbc1d1, a Rab GTPase-activating protein abundant in skeletal muscle, is partially relieved by AMP-activated protein kinase activation.
description
2008 nî lūn-bûn
@nan
2008 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@ast
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@en
type
label
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@ast
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@en
prefLabel
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@ast
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@en
P2093
P2860
P356
P1476
Inhibition of GLUT4 translocat ...... ted protein kinase activation.
@en
P2093
Gustav E Lienhard
Jose A Chavez
Susanna R Keller
William G Roach
William S Lane
P2860
P304
P356
10.1074/JBC.M708934200
P407
P577
2008-02-07T00:00:00Z