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AS160 regulates insulin- and contraction-stimulated glucose uptake in mouse skeletal muscle.
Signaling mechanisms in skeletal muscle: acute responses and chronic adaptations to exercise.
Exercise increases TBC1D1 phosphorylation in human skeletal muscle.
Insulin resistance after a 72-h fast is associated with impaired AS160 phosphorylation and accumulation of lipid and glycogen in human skeletal muscle.
Distinct signals regulate AS160 phosphorylation in response to insulin, AICAR, and contraction in mouse skeletal muscle.
Discovery of TBC1D1 as an insulin-, AICAR-, and contraction-stimulated signaling nexus in mouse skeletal muscle.
Estradiol stimulates Akt, AMP-activated protein kinase (AMPK) and TBC1D1/4, but not glucose uptake in rat soleus.
Exercise alleviates lipid-induced insulin resistance in human skeletal muscle-signaling interaction at the level of TBC1 domain family member 4.
Calmodulin-binding domain of AS160 regulates contraction- but not insulin-stimulated glucose uptake in skeletal muscle.
Identification of a novel phosphorylation site on TBC1D4 regulated by AMP-activated protein kinase in skeletal muscle.
TBC1D1 regulates insulin- and contraction-induced glucose transport in mouse skeletal muscle.
Contraction regulates site-specific phosphorylation of TBC1D1 in skeletal muscle.
Acute exercise and physiological insulin induce distinct phosphorylation signatures on TBC1D1 and TBC1D4 proteins in human skeletal muscle.
Sustained AS160 and TBC1D1 phosphorylations in human skeletal muscle 30 min after a single bout of exercise.
GTPase Activating Proteins