Saturated fatty acids inhibit induction of insulin gene transcription by JNK-mediated phosphorylation of insulin-receptor substrates. - Wikidata - wikimedia - TriplyDB

Saturated fatty acids inhibit induction of insulin gene transcription by JNK-mediated phosphorylation of insulin-receptor substrates.

Saturated fatty acids inhibit induction of insulin gene transcription by JNK-mediated phosphorylation of insulin-receptor substrates.

http://www.wikidata.org/entity/Q35133872

about

JNK Signaling: Regulation and Functions Based on Complex Protein-Protein Partnerships The Pathogenesis of Nonalcoholic Fatty Liver Disease: Interplay between Diet, Gut Microbiota, and Genetic Background Research advances in the relationship between nonalcoholic fatty liver disease and atherosclerosis Stress kinases in the modulation of metabolism and energy balance Metabolic functions of FABPs--mechanisms and therapeutic implications Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications Oxidative stress and diabetes: what can we learn about insulin resistance from antioxidant mutant mouse models?Guards and culprits in the endoplasmic reticulum: glucolipotoxicity and β-cell failure in type II diabetes Omega-3 Fatty Acids and FFAR4 Free Fatty acids and their metabolism affect function and survival of podocytes Role of p62/SQSTM1 in liver physiology and pathogenesis Fenofibrate and PBA prevent fatty acid-induced loss of adiponectin receptor and pAMPK in human hepatoma cells and in hepatitis C virus-induced steatosis Natural history of β-cell adaptation and failure in type 2 diabetes Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes Chaperoning to the metabolic party: The emerging therapeutic role of heat-shock proteins in obesity and type 2 diabetes Molecular mechanisms of chromium in alleviating insulin resistance A liver full of JNK: signaling in regulation of cell function and disease pathogenesis, and clinical approaches JNK1 protects against glucolipotoxicity-mediated beta-cell apoptosis Palmitate induces insulin resistance in H4IIEC3 hepatocytes through reactive oxygen species produced by mitochondria CDK4 is an essential insulin effector in adipocytes Serine phosphorylation sites on IRS2 activated by angiotensin II and protein kinase C to induce selective insulin resistance in endothelial cells Insulin resistance in non-obese subjects is associated with activation of the JNK pathway and impaired insulin signaling in skeletal muscle.An islet in distress: β cell failure in type 2 diabetes.Role and mechanism of pancreatic β-cell death in diabetes: The emerging role of autophagy.Glucolipotoxicity of the pancreatic beta cell.PPAR/RXR Regulation of Fatty Acid Metabolism and Fatty Acid omega-Hydroxylase (CYP4) Isozymes: Implications for Prevention of Lipotoxicity in Fatty Liver Disease Periostin promotes liver steatosis and hypertriglyceridemia through downregulation of PPARα.Palmitoleic acid prevents palmitic acid-induced macrophage activation and consequent p38 MAPK-mediated skeletal muscle insulin resistance.JNK regulation of hepatic manifestations of the metabolic syndrome.Free fatty acids in the presence of high glucose amplify monocyte inflammation via Toll-like receptors.Alteration of JNK-1 signaling in skeletal muscle fails to affect glucose homeostasis and obesity-associated insulin resistance in mice Lysophosphatidylcholine as an effector of fatty acid-induced insulin resistance.Cathepsin inhibition-induced lysosomal dysfunction enhances pancreatic beta-cell apoptosis in high glucose The chaperone balance hypothesis: the importance of the extracellular to intracellular HSP70 ratio to inflammation-driven type 2 diabetes, the effect of exercise, and the implications for clinical management.Human adipose cells in vitro are either refractory or responsive to insulin, reflecting host metabolic state Maternal obesity promotes a proinflammatory signature in rat uterus and blastocyst.Serum Immunoglobulin M Concentration Varies with Triglyceride Levels in an Adult Population: Tianjin Chronic Low-Grade Systemic Inflammation and Health (TCLSIHealth) Cohort Study.Glucolipotoxicity in Pancreatic β-Cells.Vascular smooth muscle insulin resistance, but not hypertrophic signaling, is independent of angiotensin II-induced IRS-1 phosphorylation by JNK Saturated fatty acids induce c-Src clustering within membrane subdomains, leading to JNK activation.

P2860

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P2860

Saturated fatty acids inhibit induction of insulin gene transcription by JNK-mediated phosphorylation of insulin-receptor substrates.

http://www.wikidata.org/entity/Q35133872

description

2006 nî lūn-bûn

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2006 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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2006 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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Proceedings of the National Academy of Sciences of the United States of America

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Saturated fatty acids inhibit ...... f insulin-receptor substrates.

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P2093

Francesco Galimi

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Giovanni Solinas

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Myung-Shik Lee

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Willscott Naugler

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P2860

Disruption of IRS-2 causes type 2 diabetes in mice

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

Phosphorylation of Ser307 in insulin receptor substrate-1 blocks interactions with the insulin receptor and inhibits insulin action

The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas

4PS/insulin receptor substrate (IRS)-2 is the alternative substrate of the insulin receptor in IRS-1-deficient mice

c-Jun can recruit JNK to phosphorylate dimerization partners via specific docking interactions

Involvement of c-Jun N-terminal kinase in oxidative stress-mediated suppression of insulin gene expression

Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes

The E3 ubiquitin ligase itch couples JNK activation to TNFalpha-induced cell death by inducing c-FLIP(L) turnover

Global and societal implications of the diabetes epidemic

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17050683

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phosphorylation

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1637603

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