Overexpression of a constitutively active form of phosphatidylinositol 3-kinase is sufficient to promote Glut 4 translocation in adipocytes.
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Interaction of insulin receptor substrate-1 with the sigma3A subunit of the adaptor protein complex-3 in cultured adipocytesPotential role of 3-phosphoinositide-dependent protein kinase 1 (PDK1) in insulin-stimulated glucose transporter 4 translocation in adipocytesExpression of a prenylation-deficient Rab4 inhibits the GLUT4 translocation induced by active phosphatidylinositol 3-kinase and protein kinase BLiver X receptors as insulin-mediating factors in fatty acid and cholesterol biosynthesisInsulin increases the association of Akt-2 with Glut4-containing vesiclesIdentification of the APS protein as a novel insulin receptor substrateActivation of glycogen synthase by insulin in 3T3-L1 adipocytes involves c-Cbl-associating protein (CAP)-dependent and CAP-independent signaling pathways.Munc18c regulates insulin-stimulated glut4 translocation to the transverse tubules in skeletal muscle.Diversification of cardiac insulin signaling involves the p85 alpha/beta subunits of phosphatidylinositol 3-kinase.From insulin receptor signalling to Glut 4 translocation abnormalities in obesity and insulin resistance.Protein kinase B/Akt participates in GLUT4 translocation by insulin in L6 myoblastsSpatiotemporal Regulators for Insulin-Stimulated GLUT4 Vesicle Exocytosis.Muscle-specific Pten deletion protects against insulin resistance and diabetesNormal insulin-dependent activation of Akt/protein kinase B, with diminished activation of phosphoinositide 3-kinase, in muscle in type 2 diabetesA role for protein kinase Bbeta/Akt2 in insulin-stimulated GLUT4 translocation in adipocytes.Differential regulation of phosphoinositide 3-kinase adapter subunit variants by insulin in human skeletal muscle.Regulated in development and DNA damage responses -1 (REDD1) protein contributes to insulin signaling pathway in adipocytes.Turning signals on and off: GLUT4 traffic in the insulin-signaling highway.Suppression of nuclear factor-κB activation and inflammation in microglia by physically modified saline.Potential role of Rab4 in the regulation of subcellular localization of Glut4 in adipocytes.Optogenetic activation reveals distinct roles of PIP3 and Akt in adipocyte insulin action.Inhibition of Soluble Epoxide Hydrolase Limits Mitochondrial Damage and Preserves Function Following Ischemic Injury.Involvement of phosphatidylinositol 3-kinase-mediated up-regulation of I kappa B alpha in anti-inflammatory effect of gemfibrozil in microgliaNaringenin inhibits adipogenesis and reduces insulin sensitivity and adiponectin expression in adipocytes.Hesperetin impairs glucose uptake and inhibits proliferation of breast cancer cells.Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling.Impaired activation of phosphoinositide 3-kinase by insulin in fibroblasts from patients with severe insulin resistance and pseudoacromegaly. A disorder characterized by selective postreceptor insulin resistance.Skeletal muscle insulin resistance: the interplay of local lipid excess and mitochondrial dysfunction.Phosphatidylinositol 3-phosphate [PtdIns3P] is generated at the plasma membrane by an inositol polyphosphate 5-phosphatase: endogenous PtdIns3P can promote GLUT4 translocation to the plasma membrane.Activation of phosphatidylinositol 3-kinase is sufficient for cell cycle entry and promotes cellular changes characteristic of oncogenic transformation.Insulin signaling.Insulin stimulates hypoxia-inducible factor 1 through a phosphatidylinositol 3-kinase/target of rapamycin-dependent signaling pathway.Differential effects of phosphatidylinositol 3-kinase inhibition on intracellular signals regulating GLUT4 translocation and glucose transport.Reconstitution of insulin signaling pathways in rat 3Y1 cells lacking insulin receptor and insulin receptor substrate-1. Evidence that activation of Akt is insufficient for insulin-stimulated glycogen synthesis or glucose uptake in rat 3Y1 cells.Membrane-targeted phosphatidylinositol 3-kinase mimics insulin actions and induces a state of cellular insulin resistance.Actin filaments participate in the relocalization of phosphatidylinositol3-kinase to glucose transporter-containing compartments and in the stimulation of glucose uptake in 3T3-L1 adipocytes.Effects of acutely inhibiting PI3K isoforms and mTOR on regulation of glucose metabolism in vivoInsulin and insulin-like growth factor I up-regulate GLUT4 gene expression in fetal brown adipocytes, in a phosphoinositide 3-kinase-dependent manner.Parathyroid hormone suppresses insulin signaling in adipocytes.Regulation of system A amino acid transport in 3T3-L1 adipocytes by insulin.
P2860
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P2860
Overexpression of a constitutively active form of phosphatidylinositol 3-kinase is sufficient to promote Glut 4 translocation in adipocytes.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh
1996年學術文章
@zh-hant
name
Overexpression of a constituti ...... 4 translocation in adipocytes.
@en
Overexpression of a constituti ...... 4 translocation in adipocytes.
@nl
type
label
Overexpression of a constituti ...... 4 translocation in adipocytes.
@en
Overexpression of a constituti ...... 4 translocation in adipocytes.
@nl
prefLabel
Overexpression of a constituti ...... 4 translocation in adipocytes.
@en
Overexpression of a constituti ...... 4 translocation in adipocytes.
@nl
P2093
P2860
P356
P1476
Overexpression of a constituti ...... 4 translocation in adipocytes.
@en
P2093
Grémeaux T
Le Marchand-Brustel Y
Van Obberghen E
Williams LT
P2860
P304
25227-25232
P356
10.1074/JBC.271.41.25227
P407
P577
1996-10-01T00:00:00Z