IRS1-independent defects define major nodes of insulin resistance - Wikidata - awgldk - TriplyDB

IRS1-independent defects define major nodes of insulin resistance

IRS1-independent defects define major nodes of insulin resistance

http://www.wikidata.org/entity/Q24647774

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Molecular basis of signaling specificity of insulin and IGF receptors: neglected corners and recent advances Insulin resistance is a cellular antioxidant defense mechanism JNK Signaling: Regulation and Functions Based on Complex Protein-Protein Partnerships Redox implications in adipose tissue (dys)function--A new look at old acquaintances Acetylation of TUG protein promotes the accumulation of GLUT4 glucose transporters in an insulin-responsive intracellular compartment Kinome Screen Identifies PFKFB3 and Glucose Metabolism as Important Regulators of the Insulin/Insulin-like Growth Factor (IGF)-1 Signaling Pathway Rab8A and Rab13 are activated by insulin and regulate GLUT4 translocation in muscle cells Palmitate-activated macrophages confer insulin resistance to muscle cells by a mechanism involving protein kinase C θ and ε Lysophosphatidic acid counteracts glucagon-induced hepatocyte glucose production via STAT3.Involvement of mTOR in Type 2 CRF Receptor Inhibition of Insulin Signaling in Muscle Cells.Opening of the mitochondrial permeability transition pore links mitochondrial dysfunction to insulin resistance in skeletal muscle.GLUT4 is sorted to vesicles whose accumulation beneath and insertion into the plasma membrane are differentially regulated by insulin and selectively affected by insulin resistance Molecular mechanistic associations of human diseases Cluster analysis of insulin action in adipocytes reveals a key role for Akt at the plasma membrane Dissecting the mechanism of insulin resistance using a novel heterodimerization strategy to activate Akt.A serum factor induces insulin-independent translocation of GLUT4 to the cell surface which is maintained in insulin resistance.Caveolins sequester FA on the cytoplasmic leaflet of the plasma membrane, augment triglyceride formation, and protect cells from lipotoxicity.Global phosphoproteomics identifies a major role for AKT and 14-3-3 in regulating EDC3 Lipid oversupply, selective insulin resistance, and lipotoxicity: molecular mechanisms Rab5 activity regulates GLUT4 sorting into insulin-responsive and non-insulin-responsive endosomal compartments: a potential mechanism for development of insulin resistance Palmitoleic acid prevents palmitic acid-induced macrophage activation and consequent p38 MAPK-mediated skeletal muscle insulin resistance.Palmitate-induced down-regulation of sortilin and impaired GLUT4 trafficking in C2C12 myotubes.cJun NH2-terminal kinase 1 (JNK1): roles in metabolic regulation of insulin resistance Lipid-induced insulin resistance affects women less than men and is not accompanied by inflammation or impaired proximal insulin signaling α3(V) collagen is critical for glucose homeostasis in mice due to effects in pancreatic islets and peripheral tissues Mitochondrial DNA damage and dysfunction, and oxidative stress are associated with endoplasmic reticulum stress, protein degradation and apoptosis in high fat diet-induced insulin resistance mice.Signaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis.Effects of acute lipid overload on skeletal muscle insulin resistance, metabolic flexibility, and mitochondrial performance Deletion of Cavin/PTRF causes global loss of caveolae, dyslipidemia, and glucose intolerance.Acylcarnitines: potential implications for skeletal muscle insulin resistance.The evolution of insulin resistance in muscle of the glucose infused rat The adaptor protein APPL1 increases glycogen accumulation in rat skeletal muscle through activation of the PI3-kinase signalling pathway Hyperinsulinemia leads to uncoupled insulin regulation of the GLUT4 glucose transporter and the FoxO1 transcription factor The role of the Niemann-Pick disease, type C1 protein in adipocyte insulin action.Sex differences in skeletal muscle phosphatase and tensin homolog deleted on chromosome 10 (PTEN) levels: a cross-sectional study.Lipid-overloaded enlarged adipocytes provoke insulin resistance independent of inflammation.Selective insulin resistance in adipocytes Fat-induced membrane cholesterol accrual provokes cortical filamentous actin destabilisation and glucose transport dysfunction in skeletal muscle ECM roles in the function of metabolic tissues.Acute Hepatic Insulin Resistance Contributes to Hyperglycemia in Rats Following Myocardial Infarction.

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IRS1-independent defects define major nodes of insulin resistance

http://www.wikidata.org/entity/Q24647774

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2008 nî lūn-bûn

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2008 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2008年の論文

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2008年論文

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2008年論文

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2008年论文

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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IRS1-independent defects define major nodes of insulin resistance

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J.CMET.2008.04.005

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Cell Metabolism

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IRS1-independent defects define major nodes of insulin resistance

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Anna Cederberg

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Cordula Hohnen-Behrens

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Lindsay E Wu

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Tomoyuki Yuasa

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Yousuke Ebina

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P2860

CAP defines a second signalling pathway required for insulin-stimulated glucose transport

The interaction of Akt with APPL1 is required for insulin-stimulated Glut4 translocation

A method to identify serine kinase substrates. Akt phosphorylates a novel adipocyte protein with a Rab GTPase-activating protein (GAP) domain

Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation

Insulin increases cell surface GLUT4 levels by dose dependently discharging GLUT4 into a cell surface recycling pathway

Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B

Transcriptional repression of the C/EBP-alpha and GLUT4 genes in 3T3-L1 adipocytes by tumor necrosis factor-alpha. Regulations is coordinate and independent of protein synthesis

The c-Jun NH(2)-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser(307)

Aspirin inhibits serine phosphorylation of insulin receptor substrate 1 in tumor necrosis factor-treated cells through targeting multiple serine kinases

Adipose-selective targeting of the GLUT4 gene impairs insulin action in muscle and liver

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1107654

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