Research Topics
| Jingxiang BaiSummaryAffiliation: Mount Sinai School of Medicine Country: USA Publications
Research Grants
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Detail Information
Publications
Adenovirus-mediated expression of CYP2E1 produces liver toxicity in miceJingxiang Bai
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, New York 10029, USA
Toxicol Sci 91:365-71. 2006..These results show that adenovirus-mediated overexpression of CYP2E1 could induce liver toxicity in mice and suggests a mechanism involving oxidative/nitrosative stress...
Cycloheximide protects HepG2 cells from serum withdrawal-induced apoptosis by decreasing p53 and phosphorylated p53 levelsJingxiang Bai
Department of Pharmacology and Biological Chemistry, Box 1603, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
J Pharmacol Exp Ther 319:1435-43. 2006..In summary, CHX protects HepG2 cells from serum withdrawal-induced apoptosis through inhibiting the synthesis of p53 and the phosphorylation of p53...
Overexpression of CYP2E1 in mitochondria sensitizes HepG2 cells to the toxicity caused by depletion of glutathioneJingxiang Bai
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 281:5128-36. 2006..The accumulation of CYP2E1 in hepatic mitochondria induced by ethanol consumption might play an important role in alcohol liver disease...
Adenovirus mediated overexpression of CYP2E1 increases sensitivity of HepG2 cells to acetaminophen induced cytotoxicityJingxiang Bai
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York 10029, USA
Mol Cell Biochem 262:165-76. 2004..The Ad-CYP2E1 may be useful for studies designed to investigate the role of CYP2E1 in APAP and alcoholic liver injury and to further characterize the actions and effects of CYP2E1...
Adenovirus-mediated overexpression of catalase in the cytosolic or mitochondrial compartment protects against toxicity caused by glutathione depletion in HepG2 cells expressing CYP2E1Montserrat Mari
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, New York 10029, USA
J Pharmacol Exp Ther 301:111-8. 2002..Damage to mitochondria may be a critical step for cellular toxicity by CYP2E1-derived reactive oxygen species...
Catalase protects HepG2 cells from apoptosis induced by DNA-damaging agents by accelerating the degradation of p53Jingxiang Bai
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, New York, New York 10029, USA
J Biol Chem 278:4660-7. 2003..This suggests that the level of catalase may play a critical role in cell-induced resistance to the effects of anti-cancer drugs which up-regulate p53...
Cytochrome P450 2E1 contributes to ethanol-induced fatty liver in miceYongke Lu
Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA
Hepatology 47:1483-94. 2008....
Catalase and estradiol inhibit mitochondrial protein S-glutathionylationBin Hu
Department of Medicine, The Mount Sinai School of Medicine, New York, NY 10029, USA
Mol Cell Biochem 367:51-8. 2012..This effect may play a role in ninefold greater prevalence of autoantibodies against PDC-E2 in women with primary biliary cirrhosis...
Apoptosis and the liver: relation to autoimmunity and related conditionsJingxiang Bai
Department of Pharmacology and Biological Chemistry, Mount Sinai School of Medicine, 1 G. Levy Place, P.O. Box 1123, New York, NY 10029, USA
Autoimmun Rev 2:36-42. 2003..Overexpression of anti-apoptotic proteins and FasL allow liver tumor cells to evade tumor specific cytotoxic lymphocytes. Agents that modulate apoptosis may be of future therapeutic benefit in a number of liver diseases...
Research Grants
- Overexpression of CYP2E1 and Alcohol Liver DiseaseJingxiang Bai; Fiscal Year: 2006..We hope this study could make a significant contribution to the prevention and therapy for alcohol liver disease, benefiting millions of such patients worldwide. ..
