Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity - Wikidata - wikimedia - TriplyDB

Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity

Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity

http://www.wikidata.org/entity/Q26799194

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Oxidative stress during acetaminophen hepatotoxicity: Sources, pathophysiological role and therapeutic potential TAMH: A Useful In Vitro Model for Assessing Hepatotoxic Mechanisms The Impact of Sterile Inflammation in Acute Liver Injury.Acetaminophen from liver to brain: New insights into drug pharmacological action and toxicity Benzyl alcohol protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes but causes mitochondrial dysfunction and cell death at higher doses Hearing, reactive metabolite formation, and oxidative stress in cochleae after a single acute overdose of acetaminophen: an in vivo study Tropisetron Protects Against Acetaminophen-Induced Liver Injury via Suppressing Hepatic Oxidative Stress and Modulating the Activation of JNK/ERK MAPK Pathways Role of nonalcoholic fatty liver disease as risk factor for drug-induced hepatotoxicity.Wnt/β-Catenin Signaling Drives Thioacetamide-Mediated Heteroprotection Against Acetaminophen-Induced Lethal Liver Injury.Editor's Highlight: Metformin Protects Against Acetaminophen Hepatotoxicity by Attenuation of Mitochondrial Oxidant Stress and Dysfunction.Noncoding RNAs as therapeutics for acetaminophen-induced liver injury New insights into the role and mechanism of c-Jun-N-terminal kinase signaling in the pathobiology of liver diseases.EXTRAHEPATIC TOXICITY OF ACETAMINOPHEN: CRITICAL EVALUATION OF THE EVIDENCE AND PROPOSED MECHANISMS.Modulation of O-GlcNAc levels in the liver impacts acetaminophen-induced liver injury by affecting protein adduct formation and glutathione synthesis.Sodium 4-phenylbutyric acid prevents murine acetaminophen hepatotoxicity by minimizing endoplasmic reticulum stress.Mitochondria-targeted antioxidant Mito-Tempo protects against acetaminophen hepatotoxicity.Mitochondrial-Lysosomal Axis in Acetaminophen Hepatotoxicity.

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Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity

http://www.wikidata.org/entity/Q26799194

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2015 nî lūn-bûn

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Pathophysiological significanc ...... n acetaminophen hepatotoxicity

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Pathophysiological significanc ...... n acetaminophen hepatotoxicity

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17425255.2015.1071353

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Expert Opinion on Drug Metabolism & Toxicology

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Pathophysiological significanc ...... n acetaminophen hepatotoxicity

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Hartmut Jaeschke

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Kuo Du

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Yuchao Xie

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P2860

Molecular basis for the dephosphorylation of the activation segment of the insulin receptor by protein tyrosine phosphatase 1B

Regulation of insulin-like growth factor type I (IGF-I) receptor kinase activity by protein tyrosine phosphatase 1B (PTP-1B) and enhanced IGF-I-mediated suppression of apoptosis and motility in PTP-1B-deficient fibroblasts

PTP1B regulates leptin signal transduction in vivo

Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways

Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

Mispairing C57BL/6 substrains of genetically engineered mice and wild-type controls can lead to confounding results as it did in studies of JNK2 in acetaminophen and concanavalin A liver injury

Discovery of CC-930, an orally active anti-fibrotic JNK inhibitor

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

Signal transduction by the JNK group of MAP kinases

AASLD position paper: the management of acute liver failure

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1769-1779

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3143793

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10.1517/17425255.2015.1071353

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11

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Mitchell R McGill

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pathophysiology

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