CHOP is a critical regulator of acetaminophen-induced hepatotoxicity. - Wikidata - awgldk - TriplyDB

CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

http://www.wikidata.org/entity/Q44693987

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Role of endoplasmic reticulum stress in drug-induced toxicity Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity Leukotriene C4 is the major trigger of stress-induced oxidative DNA damage Receptor interacting protein kinase 1 mediates murine acetaminophen toxicity independent of the necrosome and not through necroptosis.Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or Necrosis Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.Pharmacologic cholinesterase inhibition improves survival in acetaminophen-induced acute liver failure in the mouse CCAAT/enhancer-binding protein homologous (CHOP) protein promotes carcinogenesis in the DEN-induced hepatocellular carcinoma model Hepatitis C virus structural proteins can exacerbate or ameliorate acetaminophen-induced liver injury in mice.A Cytochrome P450-Independent Mechanism of Acetaminophen-Induced Injury in Cultured Mouse Hepatocytes Research Resource: A Reference Transcriptome for Constitutive Androstane Receptor and Pregnane X Receptor Xenobiotic Signaling Modulation of the Unfolded Protein Response by Tauroursodeoxycholic Acid Counteracts Apoptotic Cell Death and Fibrosis in a Mouse Model for Secondary Biliary Liver Fibrosis.Acetaminophen-induced liver injury in obesity and nonalcoholic fatty liver disease.Endoplasmic reticulum stress in drug- and environmental toxicant-induced liver toxicity.Sertraline induces endoplasmic reticulum stress in hepatic cells.Hydrogen-rich water protects against acetaminophen-induced hepatotoxicity in mice.Physiological/pathological ramifications of transcription factors in the unfolded protein response.Lipogenic transcription factor ChREBP mediates fructose-induced metabolic adaptations to prevent hepatotoxicity.Schlafen2 mutation unravels a role for chronic ER stress in the loss of T cell quiescence.Endoplasmic Reticulum Stress and Store-Operated Calcium Entry Contribute to Usnic Acid-Induced Toxicity in Hepatic Cells.The transcription factor CHOP, a central component of the transcriptional regulatory network induced upon CCl4 intoxication in mouse liver, is not a critical mediator of hepatotoxicity.Endoplasmic reticulum stress and MAPK signaling pathway activation underlie leflunomide-induced toxicity in HepG2 Cells.Serotonin deficiency exacerbates acetaminophen-induced liver toxicity in mice.FOXA2 alleviates CCl4-induced liver fibrosis by protecting hepatocytes in mice.C/EBP homologous protein (CHOP) contributes to hepatocyte death via the promotion of ERO1α signalling in acute liver failure.Autophagy in drug-induced liver toxicity.Endoplasmic Reticulum Stress Induction and ERK1/2 Activation Contribute to Nefazodone-Induced Toxicity in Hepatic Cells.Hepatic Amiodarone Lipotoxicity Is Ameliorated by Genetic and Pharmacological Inhibition of Endoplasmatic Reticulum Stress.Combination of tauroursodeoxycholic acid and N-acetylcysteine exceeds standard treatment for acetaminophen intoxication.Mitochondrial dysfunction induced by leflunomide and its active metabolite.xCT deficiency aggravates acetaminophen-induced hepatotoxicity under inhibition of the transsulfuration pathway.A novel spontaneous mutation in the TAP2 gene unravels its role in macrophage survival.The altered liver microRNA profile in hepatotoxicity induced by rhizome Dioscorea bulbifera in mice.Sodium 4-phenylbutyric acid prevents murine acetaminophen hepatotoxicity by minimizing endoplasmic reticulum stress.Dissecting the molecular pathophysiology of drug-induced liver injury.Bicyclol attenuates tetracycline-induced fatty liver associated with inhibition of hepatic ER stress and apoptosis in mice.Ethyl pyruvate attenuates acetaminophen-induced liver injury and prevents cellular injury induced by N-acetyl-p-benzoquinone imine.Mechanisms of acetaminophen-induced liver injury and its implications for therapeutic interventions.Calcium Signaling in Liver Injury and Regeneration

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CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

http://www.wikidata.org/entity/Q44693987

description

2013 nî lūn-bûn

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2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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2013年學術文章

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name

CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

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CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

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type

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CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

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CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

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prefLabel

CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

@en

CHOP is a critical regulator of acetaminophen-induced hepatotoxicity.

@nl

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J.JHEP.2013.04.024

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Journal of Hepatology

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CHOP is a critical regulator of acetaminophen-induced hepatotoxicity

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Angela M Valverde

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Boaz Tirosh

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Dotan Uzi

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Liran Barda

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Maya Mills

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Oren Shibolet

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Ramnik Xavier

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Ray T Chung

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Tobias Mueller

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Viviana Scaiewicz

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495-503

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scholarly article

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10.1016/J.JHEP.2013.04.024

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3

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59

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Agueda Gonzalez-rodriguez

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2013-05-09T00:00:00Z

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23665281

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