Inhibitor of apoptosis signal-regulating kinase 1 protects against acetaminophen-induced liver injury. - Wikidata - awgldk - TriplyDB

Inhibitor of apoptosis signal-regulating kinase 1 protects against acetaminophen-induced liver injury.

Inhibitor of apoptosis signal-regulating kinase 1 protects against acetaminophen-induced liver injury.

http://www.wikidata.org/entity/Q35648831

about

Acetaminophen-Induced Hepatotoxicity: a Comprehensive Update Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity Pharmacological targeting of kinases MST1 and MST2 augments tissue repair and regeneration c-Jun N-terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)-dependent pathway leading to inactivation of intramitochondrial Src.The Impact of Sterile Inflammation in Acute Liver Injury.Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.Mitochondrial protein adducts formation and mitochondrial dysfunction during N-acetyl-m-aminophenol (AMAP)-induced hepatotoxicity in primary human hepatocytes Critical review of resveratrol in xenobiotic-induced hepatotoxicity.Connexin32: a mediator of acetaminophen-induced liver injury?ASK1: a new therapeutic target for kidney disease.The role of MAP2 kinases and p38 kinase in acute murine liver injury models New insights into the role and mechanism of c-Jun-N-terminal kinase signaling in the pathobiology of liver diseases.Biochemical targets of drugs mitigating oxidative stress via redox-independent mechanisms.Quantitative Chemical Proteomic Profiling of the in Vivo Targets of Reactive Drug Metabolites.Acetaminophen Toxicity Novel Insights into Mechanisms and Future Perspectives.Dual Role of Epidermal Growth Factor Receptor in Liver Injury and Regeneration after Acetaminophen Overdose in Mice.Discovery of 2-arylquinazoline derivatives as a new class of ASK1 inhibitors.Differential susceptibility to acetaminophen-induced liver injury in sub-strains of C57BL/6 mice: 6N versus 6J.Dissecting the molecular pathophysiology of drug-induced liver injury.Mitochondrial-Lysosomal Axis in Acetaminophen Hepatotoxicity.

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Inhibitor of apoptosis signal-regulating kinase 1 protects against acetaminophen-induced liver injury.

http://www.wikidata.org/entity/Q35648831

description

2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

@zh-tw

2015年论文

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name

Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

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Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

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Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

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Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

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Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

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Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

@en

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J.TAAP.2015.03.019

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Toxicology and Applied Pharmacology

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Inhibitor of apoptosis signal- ...... minophen-induced liver injury.

@en

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Anup Ramachandran

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Anwar Farhood

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David G Breckenridge

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Hartmut Jaeschke

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John T Liles

http://www.w3.org/2001/XMLSchema#string

Margitta Lebofsky

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Yuchao Xie

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P2860

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.

ASK1 is essential for JNK/SAPK activation by TRAF2

An apoptosis signal-regulating kinase 1 inhibitor reduces cardiomyocyte apoptosis and infarct size in a rat ischemia-reperfusion model

c-Jun N-terminal kinase (JNK)-dependent acute liver injury from acetaminophen or tumor necrosis factor (TNF) requires mitochondrial Sab protein expression in mice

Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1.

Activation of apoptosis signal-regulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin.

c-Jun N-terminal kinase modulates oxidant stress and peroxynitrite formation independent of inducible nitric oxide synthase in acetaminophen hepatotoxicity.

Lysosomal iron mobilization and induction of the mitochondrial permeability transition in acetaminophen-induced toxicity to mouse hepatocytes.

Mechanisms of acetaminophen-induced cell death in primary human hepatocytes.

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10.1016/J.TAAP.2015.03.019

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2015-03-25T00:00:00Z

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25818599

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