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1. Full Text Chronic plus binge ethanol feeding synergistically induces neutrophil infiltration and liver injury in mice: A critical role for E‐selectin
by Bertola, Adeline and Park, Ogyi and Gao, Bin
Hepatology, ISSN 0270-9139, 11/2013, Volume 58, Issue 5, pp. 1814 - 1823
Chronic plus binge ethanol feeding acts synergistically to induce liver injury in mice, but the mechanisms underlying this phenomenon remain unclear. Here, we... 
PATHOGENESIS | LEUKOCYTE RECRUITMENT | A-INDUCED HEPATITIS | SEVERE ALCOHOLIC HEPATITIS | INFLAMMATION | ENDOTHELIAL-CELLS | DISEASE | ADHESION MOLECULES | GROWTH-FACTOR | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Interleukin-1beta - physiology | Liver - pathology | Humans | Mice, Inbred C57BL | Alanine Transaminase - blood | Cytochrome P-450 CYP2E1 - genetics | Neutrophil Infiltration | Liver Diseases, Alcoholic - etiology | Animals | E-Selectin - genetics | Tumor Necrosis Factor-alpha - physiology | Mice | E-Selectin - physiology | Vascular Cell Adhesion Molecule-1 - analysis | Intercellular Adhesion Molecule-1 - analysis | Leucocytes | Cytokines | Ethanol | Liver | Rodents | Hepatology | Cell adhesion & migration | Index Medicus
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2. Full Text Mammalian Mst1 and Mst2 Kinases Play Essential Roles in Organ Size Control and Tumor Suppression
by Hai Song and Kinglun Kingston and Lilia Topol and Kangsun Yun and Jianxin Hu and Lisa Garrett and Yongbin Chen and Ogyi Park and Jia Chang and R. Mark Simpson and Cun-Yu Wang and Bin Gao and Jin Jiang and Yingzi Yang and Clifford J. Tabin
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2010, Volume 107, Issue 4, pp. 1431 - 1436
Control of organ size by cell proliferation and survival is a fundamental developmental process, and its deregulation leads to cancer. However, the molecular... 
Cell growth | Phosphorylation | Hepatocytes | Cell death | Liver | Drosophila | Stem cells | Cell lines | Tumors | Apoptosis | Tumor suppressor | Hippo signaling | Yap phosphorylation | CELL CONTACT INHIBITION | PROGENITOR CELLS | GROWTH-CONTROL | HIPPO SIGNALING PATHWAY | PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | tumor suppressor | TEAD/TEF FAMILY | FEEDBACK LOOP | LIVER STEM-CELLS | TRANSCRIPTION FACTOR | PROMOTES APOPTOSIS | Proto-Oncogene Proteins - metabolism | Tumor Necrosis Factor-alpha - metabolism | Cell Line | Cell Proliferation | Liver - enzymology | Liver Neoplasms - genetics | Cell Survival | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Organ Size | Proto-Oncogene Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Liver - growth & development | Hepatocyte Growth Factor - metabolism | Animals | Cell Transformation, Neoplastic - genetics | Gene Expression Regulation, Developmental | Hepatocyte Growth Factor - genetics | Liver Neoplasms - pathology | Liver - cytology | Mice | Mutation | Liver Neoplasms - enzymology | Protein-Serine-Threonine Kinases - metabolism | Cell proliferation | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Signal transduction | Insects | Cytokines | Rodents | Kinases | Index Medicus | Biological Sciences
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3. Full Text Hepatic Hippo signaling inhibits protumoural microenvironment to suppress hepatocellular carcinoma
by Kim, Wantae and Khan, Sanjoy Kumar and Liu, Yuchen and Xu, Ruoshi and Park, Ogyi and He, Yong and Cha, Boksik and Gao, Bin and Yang, Yingzi
Gut, ISSN 0017-5749, 09/2018, Volume 67, Issue 9, pp. 1692 - 1703
ObjectiveHippo signalling is a recently identified major oncosuppressive pathway that plays critical roles in inhibiting hepatocyte proliferation, survival and... 
Inflammation | Macrophages | Liver | Cancer | Hepatocellular Carcinoma | ORGAN SIZE CONTROL | PATHWAY | INFLAMMATION | LIVER | GROWTH | TISSUE | MONOCYTE RECRUITMENT | TUMOR-ASSOCIATED MACROPHAGES | GASTROENTEROLOGY & HEPATOLOGY | CANCER | T-CELLS | Cell Proliferation - genetics | Protein-Serine-Threonine Kinases - genetics | Proto-Oncogene Proteins - genetics | Signal Transduction - genetics | Carcinoma, Hepatocellular - enzymology | Hepatocytes - metabolism | Liver Neoplasms, Experimental - therapy | Phosphoproteins - genetics | Transcription Factors - genetics | Animals | Cell Transformation, Neoplastic | Mice, Mutant Strains | Carcinoma, Hepatocellular - genetics | Hepatocyte Growth Factor - genetics | Liver Neoplasms, Experimental - enzymology | Carcinoma, Hepatocellular - therapy | Liver Neoplasms, Experimental - genetics | Mice | Protein-Serine-Threonine Kinases - metabolism | Immunohistochemistry | Flow cytometry | Phenotypes | Liver diseases | Statistical analysis | Transcription | Alcohol | Hepatocellular carcinoma | Metastasis | Mammals | Gene expression | Kinases | Yes-associated protein | Liver cancer | Signal transduction | Monocytes | Clonal deletion | Hepatocytes | Monocyte chemoattractant protein | Rodents | Genetic analysis | Monocyte chemoattractant protein 1 | Index Medicus | Abridged Index Medicus
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4. Full Text Interferon-lambda (IFN-λ) induces signal transduction and gene expression in human hepatocytes, but not in lymphocytes or monocytes
by Harold Dickensheets and Faruk Sheikh and Ogyi Park and Bin Gao and Raymond P. Donnelly
Journal of Leukocyte Biology, ISSN 0741-5400, 03/2013, Volume 93, Issue 3, pp. 377 - 385
Interferon‐alpha and interferon‐lambda induce distinct functional responses in human hepatocytes, lymphocytes, and monocytes. This study compared the ability... 
hepatitis C virus | STAT | tyrosine‐phosphorylated | IFN‐α | ISG | IFN-α | Hepatitis C virus | Tyrosine-phosphorylated | CELLS | C VIRUS-REPLICATION | ACTIVATION | CHRONIC HEPATITIS-C | TRANSCRIPTION | RECEPTOR | ALPHA | IMMUNOLOGY | IDENTIFICATION | IFN-alpha | CELL BIOLOGY | tyrosine-phosphorylated | TARGETED DISRUPTION | JAK-STAT PATHWAY | HEMATOLOGY | Interleukins - therapeutic use | Humans | Interferon-alpha - therapeutic use | Male | Monocytes - immunology | STAT Transcription Factors - immunology | Hepatitis C, Chronic - drug therapy | Hepatocytes - immunology | Hep G2 Cells | Interferon-alpha - immunology | Organ Specificity - immunology | Animals | Lymphocytes - immunology | Interleukins - immunology | Hepatitis C, Chronic - immunology | Female | Janus Kinases - immunology | Signal Transduction - physiology | Mice | Index Medicus | Receptors, Signal Transduction, & Genes
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5. Full Text In vivo consequences of liver‐specific interleukin‐22 expression in mice: Implications for human liver disease progression
by Park, Ogyi and Wang, Hua and Weng, Honglei and Feigenbaum, Lionel and Li, Hai and Yin, Shi and Ki, Sung Hwan and Yoo, Seong Ho and Dooley, Steven and Wang, Fu‐Sheng and Young, Howard A and Gao, Bin
Hepatology, ISSN 0270-9139, 07/2011, Volume 54, Issue 1, pp. 252 - 261
Interleukin‐22 (IL‐22), which acts as either a proinflammatory or anti‐inflammatory cytokine in various disease models, is markedly up‐regulated in chronic... 
CELLS | HEPATOCYTES | ACTIVATION | CYTOKINES | INFLAMMATION | MOUSE MODEL | STAT3 | GASTROENTEROLOGY & HEPATOLOGY | HEPATITIS-C | IL-22 | PSORIASIS | Liver - pathology | Hepatitis B - metabolism | Hepatitis C - metabolism | Chemical and Drug Induced Liver Injury, Chronic - metabolism | Humans | Liver Diseases - pathology | Liver Neoplasms - chemically induced | Interleukins - metabolism | Hepatectomy | Interleukins - genetics | Diethylnitrosamine - adverse effects | Liver Neoplasms - pathology | Liver - surgery | Cell Survival - physiology | Disease Models, Animal | Liver - metabolism | Mice, Inbred C57BL | Hepatitis B - pathology | Mice, Transgenic | Chemical and Drug Induced Liver Injury, Chronic - pathology | Liver Regeneration - physiology | Disease Progression | Animals | Concanavalin A - adverse effects | Liver Neoplasms - metabolism | Mice | Hepatitis C - pathology | Liver Diseases - physiopathology | Liver Diseases - metabolism | Hyperglycemia | Inflammation | Liver diseases | Cytokines | Rodents | Liver | Index Medicus
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6. Full Text Inflammation‐associated interleukin‐6/signal transducer and activator of transcription 3 activation ameliorates alcoholic and nonalcoholic fatty liver diseases in interleukin‐10–deficient mice
by Miller, Andrew M and Wang, Hua and Bertola, Adeline and Park, Ogyi and Horiguchi, Norio and Hwan Ki, Sung and Yin, Shi and Lafdil, Fouad and Gao, Bin
Hepatology, ISSN 0270-9139, 09/2011, Volume 54, Issue 3, pp. 846 - 856
Alcoholic and nonalcoholic steatohepatitis are characterized by fatty liver plus inflammation. It is generally believed that steatosis promotes inflammation,... 
LIPOTOXICITY | SIGNALING PATHWAYS | HEPATOCYTES | HEPATIC INFLAMMATION | POLYMORPHISMS | STEATOSIS | INSULIN-RESISTANCE | INJURY | NECROSIS-FACTOR-ALPHA | STEATOHEPATITIS | GASTROENTEROLOGY & HEPATOLOGY | Animals | Disease Resistance | STAT3 Transcription Factor - physiology | Fatty Liver - prevention & control | Interleukin-6 - physiology | Non-alcoholic Fatty Liver Disease | Male | Inflammation - immunology | Mice | Fatty Liver, Alcoholic - prevention & control | Sterol Regulatory Element Binding Protein 1 - physiology | Interleukin-10 - physiology | Inflammation | Cytokines | Kinases | Fatty acids | Rodents | Liver | Index Medicus
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7. Full Text Aldehyde dehydrogenase 2 deficiency ameliorates alcoholic fatty liver but worsens liver inflammation and fibrosis in mice
by Kwon, Hyo‐Jung and Won, Young‐Suk and Park, Ogyi and Chang, Binxia and Duryee, Michael J and Thiele, Geoffrey E and Matsumoto, Akiko and Singh, Surendra and Abdelmegeed, Mohamed A and Song, Byoung‐Joon and Kawamoto, Toshihiro and Vasiliou, Vasilis and Thiele, Geoffrey M and Gao, Bin
Hepatology, ISSN 0270-9139, 07/2014, Volume 60, Issue 1, pp. 146 - 157
Aldehyde dehydrogenase 2 (ALDH2) is the major enzyme that metabolizes acetaldehyde produced from alcohol metabolism. Approximately 40‐50% of East Asians carry... 
ISCHEMIA/REPERFUSION INJURY | HEPATIC STELLATE CELLS | TRANSCRIPTION 3 | METABOLISM | DISEASE | KUPFFER CELLS | KNOCKOUT MICE | ACETALDEHYDE | GASTROENTEROLOGY & HEPATOLOGY | GENE TARGETING MOUSE | SIGNAL TRANSDUCER | Acetaldehyde - metabolism | Hepatitis - enzymology | Aldehyde Dehydrogenase, Mitochondrial | Oxidative Stress - physiology | Retinal Dehydrogenase - metabolism | Male | Cytochrome P-450 CYP2E1 - metabolism | Liver Cirrhosis - enzymology | Carbon Tetrachloride Poisoning - enzymology | Fatty Liver, Alcoholic - genetics | Isoenzymes - metabolism | Hepatitis - genetics | Aldehyde Dehydrogenase - deficiency | Female | Fatty Liver, Alcoholic - enzymology | Liver Cirrhosis - genetics | Chemical and Drug Induced Liver Injury - enzymology | STAT3 Transcription Factor - metabolism | Mice, Inbred C57BL | Aldehyde Dehydrogenase - genetics | Ethanol - pharmacokinetics | Chemical and Drug Induced Liver Injury - genetics | Kupffer Cells - enzymology | Mice, Knockout | Animals | Aldehyde Dehydrogenase - blood | Carbon Tetrachloride Poisoning - genetics | Mice | Oxidative Stress - drug effects | Central Nervous System Depressants - pharmacokinetics | Dehydrogenases | Liver | Rodents | Hepatology | Index Medicus | ALDH2 | inflammation | STAT3 | fibrosis | ethanol | IL-6 | Acetaldehyde
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8. Full Text PARP inhibition protects against alcoholic and non-alcoholic steatohepatitis
by Mukhopadhyay, Partha and Horváth, Béla and Rajesh, Mohanraj and Varga, Zoltán V and Gariani, Karim and Ryu, Dongryeol and Cao, Zongxian and Holovac, Eileen and Park, Ogyi and Zhou, Zhou and Xu, Ming-Jiang and Wang, Wei and Godlewski, Grzegorz and Paloczi, Janos and Nemeth, Balazs Tamas and Persidsky, Yuri and Liaudet, Lucas and Haskó, György and Bai, Peter and Boulares, A. Hamid and Auwerx, Johan and Gao, Bin and Pacher, Pal
Journal of Hepatology, ISSN 0168-8278, 2016, Volume 66, Issue 3, pp. 589 - 600
Graphical abstract 
Gastroenterology and Hepatology | NAD | Oxidative stress | Mitochondria | Reactive oxygen species | Fatty liver | Kupffer cells | Inflammation | NASH | Alcohols | HEPATOCYTES | ACTIVATION | FATTY LIVER-DISEASE | SIRT1 | ADP-RIBOSE POLYMERASE-1 | RIBOSYLATION | METABOLISM | NAD(+) | MICE | GASTROENTEROLOGY & HEPATOLOGY | CONSUMPTION | Sirtuins | Animal models | Poly(ADP-ribose) | Mitochondrial DNA | High fat diet | Hepatitis | Cell activation | Clonal deletion | Ribose | Nutrient deficiency | Liver diseases | Methionine | Poly(ADP-ribose) polymerase | Cystic fibrosis | Metabolism | SIRT1 protein | Polymerase chain reaction | Poly(ADP-ribose) Polymerase 1 | Choline | Fibrosis | Alcoholic beverages | Cancer | Index Medicus
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9. Full Text Poly (ADP‐ribose) polymerase‐1 is a key mediator of liver inflammation and fibrosis
by Mukhopadhyay, Partha and Rajesh, Mohanraj and Cao, Zongxian and Horváth, Béla and Park, Ogyi and Wang, Hua and Erdelyi, Katalin and Holovac, Eileen and Wang, Yuping and Liaudet, Lucas and Hamdaoui, Nabila and Lafdil, Fouad and Haskó, György and Szabo, Csaba and Boulares, A. Hamid and Gao, Bin and Pacher, Pal
Hepatology, ISSN 0270-9139, 05/2014, Volume 59, Issue 5, pp. 1998 - 2009
Poly (ADP‐ribose) polymerase 1 (PARP‐1) is a constitutive enzyme, the major isoform of the PARP family, which is involved in the regulation of DNA repair, cell... 
RIBOSYLATION | POLY(ADP-RIBOSE) POLYMERASE | HEPATOCELLULAR-CARCINOMA | ACTIVATION | PHAGOCYTOSIS | HEPATIC STELLATE CELLS | PATHWAY | ADIPOCYTE FUNCTION | FIBROGENESIS | GROWTH-FACTOR | GASTROENTEROLOGY & HEPATOLOGY | Hepatitis - etiology | Hepatic Stellate Cells - physiology | Humans | Mice, Inbred C57BL | Liver Cirrhosis, Experimental - etiology | Male | Carbon Tetrachloride - toxicity | Liver Cirrhosis, Experimental - drug therapy | Poly(ADP-ribose) Polymerases - physiology | Poly(ADP-ribose) Polymerase Inhibitors | Hepatitis - drug therapy | Animals | Mice | Poly (ADP-Ribose) Polymerase-1 | Liver cirrhosis | DNA repair | Rodents | Hepatology | Index Medicus
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10. Full Text Chronic expression of interferon‐gamma leads to murine autoimmune cholangitis with a female predominance
by Bae, Heekyong R and Leung, Patrick S.C and Tsuneyama, Koichi and Valencia, Julio C and Hodge, Deborah L and Kim, Seohyun and Back, Tim and Karwan, Megan and Merchant, Anand S and Baba, Nobuyuki and Feng, Dechun and Park, Ogyi and Gao, Bin and Yang, Guo‐Xiang and Gershwin, M. Eric and Young, Howard A
Hepatology, ISSN 0270-9139, 10/2016, Volume 64, Issue 4, pp. 1189 - 1201
In most autoimmune diseases the serologic hallmarks of disease precede clinical pathology by years. Therefore, the use of animal models in defining early... 
ANTIMITOCHONDRIAL ANTIBODIES | RISK-FACTORS | EPITHELIAL-CELLS | IMMUNE-RESPONSES | PRIMARY BILIARY-CIRRHOSIS | SUSCEPTIBILITY LOCI | ANIMAL-MODELS | GASTROENTEROLOGY & HEPATOLOGY | DIFFERENTIAL GENE-EXPRESSION | T-CELLS | GENOME-WIDE ASSOCIATION | Animals | Sex Factors | Female | Male | Cholangitis - immunology | Cholangitis - metabolism | Mice | Autoimmune Diseases - etiology | Autoimmune Diseases - metabolism | Interferon-gamma - biosynthesis | Inflammation | Disease | Gene expression | Rodents | Index Medicus | autoimmune diseases | CD4 T cells | interferons | sex-biased | MHC Class II
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11. Full Text Chronic plus Binge Ethanol Feeding Synergistically Induces Neutrophil Infiltration and Liver Injury: a Critical Role for E-selectin
by Bertola, Adeline and Park, Ogyi and Gao, Bin
Hepatology (Baltimore, Md.), ISSN 0270-9139, 11/2013, Volume 58, Issue 5, pp. 1814 - 1823
We have previously demonstrated that chronic plus binge ethanol feeding acts synergistically to induce liver injury in mice; however, the mechanisms underlying... 
alcoholic liver injury | inflammation | Adhesion molecules
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12. Full Text Chronic plus binge ethanol feeding synergistically induces neutrophil infiltration and liver injury in mice: A critical role for E-selectin
: Hepatology
by Bertola, Adeline and Park, Ogyi and Gao, Bin
Hepatology, ISSN 0270-9139, 11/2013, Volume 58, Issue 5, pp. 1814 - 1823
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