Genetic disruption of AMPK signaling abolishes both contraction- and insulin-stimulated TBC1D1 phosphorylation and 14-3-3 binding in mouse skeletal muscle
about
AMP-activated protein kinase: an energy sensor that regulates all aspects of cell functionGeneral aspects of muscle glucose uptakeAMPK: a target for drugs and natural products with effects on both diabetes and cancerα-MSH Stimulates Glucose Uptake in Mouse Muscle and Phosphorylates Rab-GTPase-Activating Protein TBC1D1 Independently of AMPKContraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscleAMPK: a nutrient and energy sensor that maintains energy homeostasisRegulation of ion channels and transporters by AMP-activated kinase (AMPK).Chromium enhances insulin responsiveness via AMPK.In vivo exercise followed by in vitro contraction additively elevates subsequent insulin-stimulated glucose transport by rat skeletal muscle.Insulin signaling, resistance, and the metabolic syndrome: insights from mouse models into disease mechanisms.TBC1D1 regulates insulin- and contraction-induced glucose transport in mouse skeletal muscle.Mechanism of action of compound-13: an α1-selective small molecule activator of AMPKEMG-normalised kinase activation during exercise is higher in human gastrocnemius compared to soleus muscle.High-fat and obesogenic diets: current and future strategies to fight obesity and diabetes.The Murphy Roths Large (MRL) mouse strain is naturally resistant to high fat diet-induced hyperglycemiaRoles of TBC1D1 and TBC1D4 in insulin- and exercise-stimulated glucose transport of skeletal muscleStructural and population-based evaluations of TBC1D1 p.Arg125TrpExercise increases TBC1D1 phosphorylation in human skeletal muscle.AMP-activated protein kinase (AMPK) beta1beta2 muscle null mice reveal an essential role for AMPK in maintaining mitochondrial content and glucose uptake during exercise.Insulin inhibits AMPK activity and phosphorylates AMPK Ser⁴⁸⁵/⁴⁹¹ through Akt in hepatocytes, myotubes and incubated rat skeletal muscle.Sirtuin3 Dysfunction Is the Key Determinant of Skeletal Muscle Insulin Resistance by Angiotensin IIExercise alleviates lipid-induced insulin resistance in human skeletal muscle-signaling interaction at the level of TBC1 domain family member 4.AMPK and Exercise: Glucose Uptake and Insulin Sensitivity.Regulatory mode shift of Tbc1d1 is required for acquisition of insulin-responsive GLUT4-trafficking activity.LKB1 regulates lipid oxidation during exercise independently of AMPKInsulin stimulation regulates AS160 and TBC1D1 phosphorylation sites in human skeletal muscleInsulin 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 phosphorylationAmino-4-imidazolecarboxamide ribotide directly inhibits coenzyme A biosynthesis in Salmonella enterica.Energy sensing by the AMP-activated protein kinase and its effects on muscle metabolism.Re-evaluating the general(ized) roles of AMPK in cellular metabolism.Current understanding of increased insulin sensitivity after exercise - emerging candidates.Mapping insulin/GLUT4 circuitry.AMP-activated protein kinase: an emerging drug target to regulate imbalances in lipid and carbohydrate metabolism to treat cardio-metabolic diseasesAMPK-sensitive cellular transport.AMP-activated protein kinase: a key regulator of energy balance with many roles in human disease.AMP-activated protein kinase: maintaining energy homeostasis at the cellular and whole-body levels.PT-1 selectively activates AMPK-γ1 complexes in mouse skeletal muscle, but activates all three γ subunit complexes in cultured human cells by inhibiting the respiratory chain.Targeting of AMP-activated protein kinase: prospects for computer-aided drug design.Regulation of Carbohydrate Metabolism, Lipid Metabolism, and Protein Metabolism by AMPK.
P2860
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P2860
Genetic disruption of AMPK signaling abolishes both contraction- and insulin-stimulated TBC1D1 phosphorylation and 14-3-3 binding in mouse skeletal muscle
description
2009 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2009 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2009
@ast
scientific journal article
@en
vedecký článok (publikovaný 2009/09/01)
@sk
vědecký článek publikovaný v roce 2009
@cs
wetenschappelijk artikel (gepubliceerd op 2009/09/01)
@nl
наукова стаття, опублікована у вересні 2009
@uk
مقالة علمية (نشرت في سبتمبر 2009)
@ar
name
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@ast
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@en
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@nl
type
label
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@ast
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@en
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@nl
prefLabel
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@ast
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@en
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@nl
P2093
P2860
P50
P921
P3181
P1476
Genetic disruption of AMPK sig ...... nding in mouse skeletal muscle
@en
P2093
Christian Pehmøller
D. Grahame Hardie
Jørgen F. P. Wojtaszewski
Shuai Chen
P2860
P304
P3181
P356
10.1152/AJPENDO.00115.2009
P577
2009-09-01T00:00:00Z