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Cell Death and Cell Death Responses in Liver Disease: Mechanisms and Clinical Relevance

Gastroenterology (New York, N.Y. 1943), 2014-10, Vol.147 (4), p.765-783.e4

2014

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Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or Necrosis

International journal of molecular sciences, 2017-05, Vol.18 (5), p.1018

2017

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The contribution of endoplasmic reticulum stress to liver diseases

Hepatology (Baltimore, Md.), 2011-05, Vol.53 (5), p.1752-1763

2011

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Glutathione in liver diseases and hepatotoxicity

Molecular aspects of medicine, 2009-02, Vol.30 (1), p.29-41

2009

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EASL Clinical Practice Guidelines: Drug-induced liver injury

Journal of hepatology, 2019-06, Vol.70 (6), p.1222-1261

2019

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Mechanisms of drug-induced liver injury

Clinics in liver disease, 2013-11, Vol.17 (4), p.507-518

2013

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c‐Jun N‐terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)‐dependent pathway leading to inactivation of intramitochondrial Src

Hepatology (Baltimore, Md.), 2016-06, Vol.63 (6), p.1987-2003

2016

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The Regulation of JNK Signaling Pathways in Cell Death through the Interplay with Mitochondrial SAB and Upstream Post-Translational Effects

International journal of molecular sciences, 2018-11, Vol.19 (11), p.3657

2018

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Mechanisms of adaptation and progression in idiosyncratic drug induced liver injury, clinical implications

Liver international, 2016-02, Vol.36 (2), p.158-165

2016

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Gut microbiota mediates diurnal variation of acetaminophen induced acute liver injury in mice

Journal of hepatology, 2018-07, Vol.69 (1), p.51-59

2018

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Acetaminophen hepatoxicity: What do we know, what don't we know, and what do we do next?

Hepatology (Baltimore, Md.), 2004-07, Vol.40 (1), p.23-26

Kaplowitz, Neil

2004

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c-Jun N-terminal Kinase (JNK)-dependent Acute Liver Injury from Acetaminophen or Tumor Necrosis Factor (TNF) Requires Mitochondrial Sab Protein Expression in Mice

The Journal of biological chemistry, 2011-10, Vol.286 (40), p.35071-35078

2011

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Inhibition of immune tolerance unmasks drug‐induced allergic hepatitis

Hepatology (Baltimore, Md.), 2015-08, Vol.62 (2), p.346-348

2015

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Role of JNK Translocation to Mitochondria Leading to Inhibition of Mitochondria Bioenergetics in Acetaminophen-induced Liver Injury

The Journal of biological chemistry, 2008-05, Vol.283 (20), p.13565-13577

2008

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Death and liver transplantation within 2 years of onset of drug‐induced liver injury

Hepatology (Baltimore, Md.), 2017-10, Vol.66 (4), p.1275-1285

2017

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Sab (Sh3bp5) dependence of JNK mediated inhibition of mitochondrial respiration in palmitic acid induced hepatocyte lipotoxicity

Journal of hepatology, 2015-06, Vol.62 (6), p.1367-1374

2015

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Mechanisms of liver injury. III. Role of glutathione redox status in liver injury

American journal of physiology: Gastrointestinal and liver physiology, 2006-07, Vol.291 (1), p.G1-G7

2006

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Regulation of drug-induced liver injury by signal transduction pathways: critical role of mitochondria

Trends in pharmacological sciences (Regular ed.), 2013-04, Vol.34 (4), p.243-253

2013

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Regulation of Mitochondrial Glutathione Redox Status and Protein Glutathionylation by Respiratory Substrates

The Journal of biological chemistry, 2010-12, Vol.285 (51), p.39646-39654

2010

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Mitochondrial glutathione: Features, regulation and role in disease

Biochimica et biophysica acta, 2013-05, Vol.1830 (5), p.3317-3328

2013

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Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through c‐jun‐N‐terminal kinase (JNK)‐dependent and ‐independent signaling pathways

Hepatology (Baltimore, Md.), 2014-04, Vol.59 (4), p.1543-1554

2014

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Introducing Laurie DeLeve, M.D., Ph.D., Our 2022 AASLD President

Hepatology (Baltimore, Md.), 2022-03, Vol.75 (3), p.514-517

Kaplowitz, Neil

2022

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Hyperhomocysteinemia, endoplasmic reticulum stress, and alcoholic liver injury

World journal of gastroenterology : WJG, 2004-06, Vol.10 (12), p.1699

2004

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Protective role of p53 in acetaminophen hepatotoxicity

Free radical biology & medicine, 2017-05, Vol.106, p.111-117

2017

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Questions and controversies: the role of necroptosis in liver disease

Cell death discovery, 2016-12, Vol.2 (1), p.16089-16089, Article 16089

2016

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Cell Death and Cell Death Responses in Liver Disease: Mechanisms and Clinical Relevance

Drug-Induced Liver Injury: Cascade of Events Leading to Cell Death, Apoptosis or Necrosis

The contribution of endoplasmic reticulum stress to liver diseases

Glutathione in liver diseases and hepatotoxicity

EASL Clinical Practice Guidelines: Drug-induced liver injury

Mechanisms of drug-induced liver injury

c‐Jun N‐terminal kinase mediates mouse liver injury through a novel Sab (SH3BP5)‐dependent pathway leading to inactivation of intramitochondrial Src

The Regulation of JNK Signaling Pathways in Cell Death through the Interplay with Mitochondrial SAB and Upstream Post-Translational Effects

Mechanisms of adaptation and progression in idiosyncratic drug induced liver injury, clinical implications

Gut microbiota mediates diurnal variation of acetaminophen induced acute liver injury in mice

Acetaminophen hepatoxicity: What do we know, what don't we know, and what do we do next?

c-Jun N-terminal Kinase (JNK)-dependent Acute Liver Injury from Acetaminophen or Tumor Necrosis Factor (TNF) Requires Mitochondrial Sab Protein Expression in Mice

Inhibition of immune tolerance unmasks drug‐induced allergic hepatitis

Role of JNK Translocation to Mitochondria Leading to Inhibition of Mitochondria Bioenergetics in Acetaminophen-induced Liver Injury

Death and liver transplantation within 2 years of onset of drug‐induced liver injury

Sab (Sh3bp5) dependence of JNK mediated inhibition of mitochondrial respiration in palmitic acid induced hepatocyte lipotoxicity

Mechanisms of liver injury. III. Role of glutathione redox status in liver injury

Regulation of drug-induced liver injury by signal transduction pathways: critical role of mitochondria

Regulation of Mitochondrial Glutathione Redox Status and Protein Glutathionylation by Respiratory Substrates

Mitochondrial glutathione: Features, regulation and role in disease

Protein kinase C (PKC) participates in acetaminophen hepatotoxicity through c‐jun‐N‐terminal kinase (JNK)‐dependent and ‐independent signaling pathways

Introducing Laurie DeLeve, M.D., Ph.D., Our 2022 AASLD President

Hyperhomocysteinemia, endoplasmic reticulum stress, and alcoholic liver injury

Protective role of p53 in acetaminophen hepatotoxicity

Questions and controversies: the role of necroptosis in liver disease

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