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Defeng Wu

  • ASSOCIATE PROFESSOR Pharmacology and Systems Therapeutics
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Education

  • B.S., Fujian Medical College
    Medicine

  • First Hospital Affiliated with Fujian Medical College, Fuzhou Hospital for Infectious Diseases
    Infectious Diseases

  • M.S., Cancer Institute, Beijing Union Medical College
    Chemical Carcinogenesis and Tumor Genetics, National Laboratory of Molecular Oncology

  • Ph.D., Cancer Institute, Beijing Union Medical College
    Biochemical Toxicology and Tumor Cell Biology, National Laboratory of Molecular Oncology

  • Mount Sinai School of Medicine
    Department of Biochemistry

Biography

    Dr. Wu is a Research Associate Professor in the Cederbaum Laboratory in the Department of Pharmacology and Systems Therapeutics.

Awards

  • 1988 -
    The Second Prize of Advantage Award
    National Health Science and Technology, China

  • 1982 -
    The Second Prize of Chinese National Natural Science Award

Publications

Wu D, Cederbaum A. Activation of ASK-1 and downstream MAP kinases in cytochrome P4502E1 potentiated tumor necrosis factor alpha liver injury. Free Radic Biol Med 2010 Aug; 49(3): 348-360.

Cederbaum AI, Lu Y, Wu D. Role of oxidative stress in alcohol-induced liver injury. Arch Toxicol 2009 Jun; 83(6): 519-548.

Wu D, Xu C, Cederbaum A. Role of nitric oxide and nuclear factor-kappaB in the CYP2E1 potentiation of tumor necrosis factor alpha hepatotoxicity in mice. Free Radic Biol Med 2009 Feb; 46(4): 480-491.

Wu D, Cederbaum AI. Development and properties of HepG2 cells that constitutively express CYP2E1. Methods Mol Biol 2008; 447: 137-150.

Wu D, Cederbaum A. Cytochrome P4502E1 sensitizes to tumor necrosis factor alpha-induced liver injury through activation of mitogen-activated protein kinases in mice. Hepatology 2008 March; 47(3): 1005-1117.

Jimenez-Lopez JM, Wu D, Cederbaum AI. Synergistic toxicity induced by prolonged glutathione depletion and inhibition of nuclear factor-kappaB signaling in liver cells. Toxicol In Vitro 2008 Feb; 22(1): 106-115.

Wu D, Cederbaum A. Nitric oxide donors prevent while the nitric oxide synthase inhibitor L-NAME increases arachidonic acid plus CYP2E1-dependent toxicity. Toxicol Appl Pharmacol 2006 Oct; 216(2): 282-292.

Wu D, Cederbaum AI. Opposite action of S-adenosyl methionine and its metabolites on CYP2E1-mediated toxicity in pyrazole-induced rat hepatocytes and HepG2 E47 cells. Am J Physiol Gastrointest Liver Physiol 2006 Apr; 290(4): 674-684.

Wu D, Cederbaum AI. Oxidative stress mediated toxicity exerted by ethanol-inducible CYP2E1. Toxicol Appl Pharmacol 2005 Sep 1; 207(2 Suppl): 70-76.

Wu D, Cederbaum AI. Alcohol, oxidative stress, and free radical damage. Alcohol Res Health 2003; 27(4): 277-284.

Industry Relationships

Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.

Dr. Wu did not report having any of the following types of financial relationships with industry during 2012 and/or 2013: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.

Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.

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