Mice with AS160/TBC1D4-Thr649Ala knockin mutation are glucose intolerant with reduced insulin sensitivity and altered GLUT4 trafficking. - Wikidata - awgldk - TriplyDB

Mice with AS160/TBC1D4-Thr649Ala knockin mutation are glucose intolerant with reduced insulin sensitivity and altered GLUT4 trafficking.

Mice with AS160/TBC1D4-Thr649Ala knockin mutation are glucose intolerant with reduced insulin sensitivity and altered GLUT4 trafficking.

http://www.wikidata.org/entity/Q34837082

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α-MSH Stimulates Glucose Uptake in Mouse Muscle and Phosphorylates Rab-GTPase-Activating Protein TBC1D1 Independently of AMPK AS160 phosphotyrosine-binding domain constructs inhibit insulin-stimulated GLUT4 vesicle fusion with the plasma membrane AMPK: a nutrient and energy sensor that maintains energy homeostasis Rab GAPs AS160 and Tbc1d1 play nonredundant roles in the regulation of glucose and energy homeostasis in mice Deletion of Rab GAP AS160 modifies glucose uptake and GLUT4 translocation in primary skeletal muscles and adipocytes and impairs glucose homeostasis.Postexercise improvement in insulin-stimulated glucose uptake occurs concomitant with greater AS160 phosphorylation in muscle from normal and insulin-resistant rats.Leptin reduces the expression and increases the phosphorylation of the negative regulators of GLUT4 traffic TBC1D1 and TBC1D4 in muscle of ob/ob mice.Expression and phosphorylation of the AS160_v2 splice variant supports GLUT4 activation and the Warburg effect in multiple myeloma.Effects of exercise on AMPK signaling and downstream components to PI3K in rat with type 2 diabetes.Roles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscle AMPK and insulin action--responses to ageing and high fat diet.AMP-activated protein kinase (AMPK) beta1beta2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise.PKB-Mediated Thr649 Phosphorylation of AS160/TBC1D4 Regulates the R-Wave Amplitude in the Heart AMPK-TBC1D4-dependent mechanism for increasing insulin sensitivity of skeletal muscle Insulin and AMPK regulate FA translocase/CD36 plasma membrane recruitment in cardiomyocytes via Rab GAP AS160 and Rab8a Rab GTPase Organismal carbohydrate and lipid homeostasis.Lipid-induced Muscle Insulin Resistance Is Mediated by GGPPS via Modulation of the RhoA/Rho Kinase Signaling Pathway.The insulin response integrates increased TGF-β signaling through Akt-induced enhancement of cell surface delivery of TGF-β receptors.AMPK and Exercise: Glucose Uptake and Insulin Sensitivity.Regulatory mode shift of Tbc1d1 is required for acquisition of insulin-responsive GLUT4-trafficking activity.Insulin signalling mechanisms for triacylglycerol storage.AS160 deficiency causes whole-body insulin resistance via composite effects in multiple tissues Insulin stimulation regulates AS160 and TBC1D1 phosphorylation sites in human skeletal muscle SEC16A is a RAB10 effector required for insulin-stimulated GLUT4 trafficking in adipocytes.TDP-43, an ALS linked protein, regulates fat deposition and glucose homeostasis.Specialized sorting of GLUT4 and its recruitment to the cell surface are independently regulated by distinct Rabs.AS160 controls eukaryotic cell cycle and proliferation by regulating the CDK inhibitor p21 Insulin resistance after a 72-h fast is associated with impaired AS160 phosphorylation and accumulation of lipid and glycogen in human skeletal muscle.Immobilization rapidly induces muscle insulin resistance together with the activation of MAPKs (JNK and p38) and impairment of AS160 phosphorylation Impairments in site-specific AS160 phosphorylation and effects of exercise training.Insulin-induced Effects on the Subcellular Localization of AKT1, AKT2 and AS160 in Rat Skeletal Muscle.Current understanding of increased insulin sensitivity after exercise - emerging candidates.Mapping insulin/GLUT4 circuitry.Akt/PKB activation and insulin signaling: a novel insulin signaling pathway in the treatment of type 2 diabetes.AMP-activated protein kinase: a key regulator of energy balance with many roles in human disease.Protein phosphatase 2A (PP2A)-specific ubiquitin ligase MID1 is a sequence-dependent regulator of translation efficiency controlling 3-phosphoinositide-dependent protein kinase-1 (PDPK-1).Evolution of signal multiplexing by 14-3-3-binding 2R-ohnologue protein families in the vertebrates.Thr649Ala-AS160 knock-in mutation does not impair contraction/AICAR-induced glucose transport in mouse muscle Ginsenoside Rb1 increases insulin sensitivity by activating AMP-activated protein kinase in male rats.14-3-3ζ: A numbers game in adipocyte function?

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Mice with AS160/TBC1D4-Thr649Ala knockin mutation are glucose intolerant with reduced insulin sensitivity and altered GLUT4 trafficking.

http://www.wikidata.org/entity/Q34837082

description

2011 nî lūn-bûn

@nan

2011 թուականի Յունուարին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի հունվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking.

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J.CMET.2010.12.005

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Cell Metabolism

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Mice with AS160/TBC1D4-Thr649A ...... and altered GLUT4 trafficking

@en

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David H Wasserman

http://www.w3.org/2001/XMLSchema#string

Kei Sakamoto

http://www.w3.org/2001/XMLSchema#string

Shuai Chen

http://www.w3.org/2001/XMLSchema#string

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Substrate specificity and effect on GLUT4 translocation of the Rab GTPase-activating protein Tbc1d1

Insulin-regulatable tissues express a unique insulin-sensitive glucose transport protein

Rapid activation of Akt2 is sufficient to stimulate GLUT4 translocation in 3T3-L1 adipocytes

Rab10, a target of the AS160 Rab GAP, is required for insulin-stimulated translocation of GLUT4 to the adipocyte plasma membrane

Insulin-stimulated cytosol alkalinization facilitates optimal activation of glucose transport in cardiomyocytes

Cell surface labeling of glucose transporter isoform GLUT4 by bis-mannose photolabel. Correlation with stimulation of glucose transport in rat adipose cells by insulin and phorbol ester

Insulin-stimulated phosphorylation of the Rab GTPase-activating protein TBC1D1 regulates GLUT4 translocation

Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta)

Inhibition of GLUT4 translocation by Tbc1d1, a Rab GTPase-activating protein abundant in skeletal muscle, is partially relieved by AMP-activated protein kinase activation.

Direct quantification of fusion rate reveals a distal role for AS160 in insulin-stimulated fusion of GLUT4 storage vesicles.

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68-79

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scholarly article

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10.1016/J.CMET.2010.12.005

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1

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13

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Carol MacKintosh

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2011-01-01T00:00:00Z

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49718431

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21195350

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3081066

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