Associate Professor, Dept. Molecular Cell Biology, School of Natural Sciences
School of Natural Sciences
Office Phone: (209) 228-4386
- Understanding the role of oxidative stress in viral infections
- Interaction of ethanol and hepatitis C virus (HCV)
- Mechanisms of chemical-biological and virus-host interactions to identify novel targets for therapy
- Mechanism and function of alternate frames decoding during HCV infection
Recent findings from Professor Choi's laboratory suggest that:
- HCV induces oxidative stress by elevating NAD(P)H oxidase 1 and 4 expression in hepatocytes
- Redox modulation has significant effects on HCV
- Oxidative stress is likely to promote the development of liver diseases, including hepatocellular carcinoma
- Ethanol, an important cofactor in liver diseases, elevates complete replication of HCV at physiologically relevant doses by elevating NADH/NAD+ ratio and lipid metabolism
- F protein (also known as ARFP, Core+1/F, and p17) has important biological functions during HCV infection
Profess Choi has studies in progress to define the underlying mechanisms as well as in vivo relevance of these findings.
Choi, J. Oxidative stress, endogenous antioxidants, alcohol, and hepatitis C: pathogenic interactions and therapeutic implications. Free Radical Biology & Medicine 52(7):1135-1150, 2012.
Seronello, S.; Montanez, J.; Presleigh, K.; Barlow, M.; Park, S.B.; and Choi, J. Ethanol and reactive species increase basal sequence heterogeneity of hepatitis C virus RNA and produce variants with reduced susceptibility to antivirals. PLoS One 6(11):327436, 2011.
Reyes de Mochel, S.N., Seronello, S., Wang, S.H., Ito, C., Zheng, J., Liang, T.J., Lambeth, D.R., Choi, J. (2010). Hepatocyte NAD(P)H oxidases as an endogenous source of reactive oxygen species during hepatitis C virus infection. Hepatology, DOI 10.1002/hep.23671. (Featured in MDLinx.com in May 2010 and Bay Bio Report 2011. Also featured by the Target Intelligence Service.com in July 2010 (Case Report 39093) and in Biological Research Information Center (BRIC) website, March 2010.).
Liu, R.-M., Choi, J., Wu, J.-H., Gaston Pravia, K.A., Lewis, K.M., Brand, J.D., Reyes Mochel, N.S., Krzywanski, D.M., Lambeth, J.D., Hagood, J.S., Forman, H. J., Thannickal, V.J., Postlethwait, E.M. (2010). Oxidative Modification of Nuclear Mitogen-activated Protein Kinase Phosphatase 1 Is Involved in Transforming Growth Factor β1-induced Expression of Plasminogen Activator Inhibitor 1 in Fibroblasts. The Journal of Biological Chemistry, 285(21), 16239.
Seronello, S., Ito, C., Wakita, T., Choi, J. (2010). Ethanol Enhances Hepatitis C Virus Replication through Lipid Metabolism and Elevated NADH/NAD+. The Journal of Biological Chemistry, 285, 845-854. DOI10.1074/jbc.M109.045740.
Sir, D., Chen, W.-L., Choi, J., Wakita, T., Yen, T.S.B., Ou, J.-H. (2008). Hepatitis C virus induces autophagy via the induction of endoplasmic reticulum stress. Hepatology, 48, 1054-1061. ([Commentary (Editor's Choice) appeared in Science 321:1135, 2008: "Hitchhiking in Membrane Traffic," by Chin, G; and Yeston, J., eds.]).
Sheikh, M., Choi, J., Qadri, I., Friedman, J.E., Sanyal, A.J. (2008). HCV infection: molecular pathways to metabolic syndrome. Hepatology, 47(6), 2127-2133.
Seronello, S., Sheikh, M.Y., Choi, J. (2007). Redox regulation of hepatitis C in non-alcoholic and alcoholic liver. Free Radical Biology & Medicine, 43(6), 869-882.
Choi, J., Forman, H.J., Ou, J.H., Lai, M.M.C., Seronello, S., Nandipati, A. (2006). Redox modulation of hepatitis C virus replication complex is calcium dependent. Free Radical Biology & Medicine, 41, 1488-1498.
Choi, J., Ou, J.H. (2006). Mechanisms of Liver Injury. III. Oxidative stress in the pathogenesis of hepatitis C virus. American Journal of Physiology, Gastrointestinal and Liver Physiology, 290, 847-851.
Choi, J., Yi, K.J., Yan, Y., Lai, M.M.C., Ou, J.H. (2004). Reactive oxygen species suppress hepatitis C virus RNA replication in human hepatoma cells. Hepatology, 33, 89-93.
Choi, J., Xu, Z., Ou, J.H. (2003). Triple decoding of hepatitis C virus core protein coding sequence by translational frameshifting. Molecular and Cellular Biology, 23(5), 1489-1497.
Xu, Z., Choi, J., Benedict Yen, T.S., Lu, W., Strohecker, A., Govindarajan, S., Selby, M.J., Ou, J.-H. (2001). Synthesis of a novel hepatitis C virus protein by ribosomal frameshift. EMBO Journal, 20(14), 3840-3848.
Choi, J., Liu, R.M., Sangiorgi, F., Wu, W., Maxson, R., Forman, H.J. (2000). Molecular mechanism of decreased glutathione content in human immunodeficiencey virus type 1 Tat transgenic mice. Journal of Biological Chemistry, 275(5), 3693-3698.
Kaul, N., Choi, J., Forman, H. J. (1998). Transmembrane redox signaling activates NF-kB in macrophages. Free Radical Biology in medicine, 24(1), 202-207.
Choi, J., Liu, R.M., Forman, H. J. (1997). Adaptation to oxidative stress: protection of signaling in rat lung epithelial L2 cells by quinone. Biochemical Pharmacology, 53(7), 987-993