c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
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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 injuryMechanisms of acetaminophen-induced liver necrosisAcetaminophen-induced Liver Injury: from Animal Models to HumansMesenchymal stromal cell therapy in liver disease: opportunities and lessons to be learnt?Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicityXenobiotic and Endobiotic Mediated Interactions Between the Cytochrome P450 System and the Inflammatory Response in the LiverMitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modificationsMechanisms of drug-induced liver injuryToll like receptor 3 plays a critical role in the progression and severity of acetaminophen-induced hepatotoxicityEvidence-based selection of training compounds for use in the mechanism-based integrated prediction of drug-induced liver injury in manQuestions and controversies: the role of necroptosis in liver diseaseMolecular mechanisms of liver injury and hepatocarcinogenesis: focusing on the role of stress-activated MAPKInflammation- and stress-related signaling pathways in hepatocarcinogenesisA liver full of JNK: signaling in regulation of cell function and disease pathogenesis, and clinical approachesChronic Deletion and Acute Knockdown of Parkin Have Differential Responses to Acetaminophen-induced Mitophagy and Liver Injury in MiceOral methylthioadenosine administration attenuates fibrosis and chronic liver disease progression in Mdr2-/- miceHumanizing π-class glutathione S-transferase regulation in a mouse model alters liver toxicity in response to acetaminophen overdoseCREBH determines the severity of sulpyrine-induced fatal shockc-Jun N-terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)-dependent pathway leading to inactivation of intramitochondrial Src.Receptor interacting protein kinase 1 mediates murine acetaminophen toxicity independent of the necrosome and not through necroptosis.c-Jun N-terminal kinase (JNK)-dependent acute liver injury from acetaminophen or tumor necrosis factor (TNF) requires mitochondrial Sab protein expression in miceIcam-1 upregulation in ethanol-induced Fatty murine livers promotes injury and sinusoidal leukocyte adherence after transplantation.Hepatic FcRn regulates albumin homeostasis and susceptibility to liver injuryGentiana manshurica Kitagawa prevents acetaminophen-induced acute hepatic injury in mice via inhibiting JNK/ERK MAPK pathwayOxidative stress promotes D-GalN/LPS-induced acute hepatotoxicity by increasing glycogen synthase kinase 3β activity.Redox regulation of tumor necrosis factor signalingAcetaminophen reactive intermediates target hepatic thioredoxin reductaseInhibition of hepatic mitochondrial aldehyde dehydrogenase by carbon tetrachloride through JNK-mediated phosphorylation.Silencing glycogen synthase kinase-3beta inhibits acetaminophen hepatotoxicity and attenuates JNK activation and loss of glutamate cysteine ligase and myeloid cell leukemia sequence 1.Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or NecrosisHepatoprotective Effect of Polyphenol-Enriched Fraction from Folium Microcos on Oxidative Stress and Apoptosis in Acetaminophen-Induced Liver Injury in MiceChronic intermittent hypoxia and acetaminophen induce synergistic liver injury in mice.Redox control of liver function in health and diseaseThe Impact of Sterile Inflammation in Acute Liver Injury.Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.CYP2E1 potentiation of LPS and TNFα-induced hepatotoxicity by mechanisms involving enhanced oxidative and nitrosative stress, activation of MAP kinases, and mitochondrial dysfunction.c-Jun N-terminal kinase modulates oxidant stress and peroxynitrite formation independent of inducible nitric oxide synthase in acetaminophen hepatotoxicity.Differential regulation of mitogen-activated protein kinase pathways by acetaminophen and its nonhepatotoxic regioisomer 3'-hydroxyacetanilide in TAMH cells.Mechanisms of acetaminophen-induced cell death in primary human hepatocytes.Serum mitochondrial biomarkers and damage-associated molecular patterns are higher in acetaminophen overdose patients with poor outcome.
P2860
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P2860
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年学术文章
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2006年学术文章
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2006年学术文章
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2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
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2006年學術文章
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name
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@en
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@nl
type
label
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@en
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@nl
prefLabel
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@en
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@nl
P2093
P1433
P1476
c-Jun N-terminal kinase plays a major role in murine acetaminophen hepatotoxicity.
@en
P2093
Basuki K Gunawan
Derick Han
Naoko Hanawa
Neil Kaplowitz
William A Gaarde
Zhang-Xu Liu
P304
P356
10.1053/J.GASTRO.2006.03.045
P407
P577
2006-07-01T00:00:00Z