个人简历

B.S., Idaho State University, Microbiology, 1995
Ph.D., Washington State University, Pharmacology/Toxicology, 2003
Postdoctoral Fellow, NIH/NRSA Fellowship, University of Texas Medical Branch, Molecular Pharmacology, 2003-07

近期论文

Lamb C. L., Cholico, G. N., Pu, X., Hagler, G. D., Cornell, K. A., and Mitchell, K. A. (2016) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) increases necroinflammation and hepatic stellate cell activation but does not exacerbate experimental liver fibrosis in mice. Toxicol. Appl. Pharmacol. Sep 28 (16)30291-5.
Lamb, C. L., Cholico, G. N., Perkins, D. E., Fewkes, M. T., Oxford, J. T., Lujan, T. J., Morrill, E. E., and Mitchell, K. A. (2016) Aryl hydrocarbon receptor activation by TCDD modulates expression of extracellular matrix remodeling genes during experimental liver fibrosis. BioMed. Res. Int. 2016:5309328. http://dx.doi.org/10.1155/2016/5309328
Wyler, S. L., D’Ingillo, S. L., Lamb, C. L., Mitchell, K. A. (2016) Monocyte chemoattractant protein-1 is not required for liver regeneration after partial hepatectomy. J. Inflamm. (Lond.) 13(1):28. http://www.journal–inflammation.com/content/13/1/28
Harvey, W. A., Jurgensen, K., Pu, X., Lamb, C. L., Cornell, K. A., Clark, R. J., Klocke, C., and Mitchell, K. A. (2016) Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increases human hepatic stellate cell activation. Toxicology 17(344-346):26-33.
Jackson, D. P, Li, H., Mitchell, K. A., Joshi, A. D., and Elferink, C. J. (2014) Ah receptor-mediated suppression of liver regeneration through NC-XRE-driven p21Cip1 expression. Mol. Pharmacol. 85(4):533-41.
Horras, C. J., Lamb, C. L., King, A. L., Hanley, J. R. and Mitchell, K. A. (2012 ) Consequences of TCDD treatment on intrahepatic lymphocytes during liver regeneration. J. Immunotoxicol. 9(4):359-67.
Horras, C. J., Lamb, C. L. and Mitchell, K. A. (2011) Regulation of hepatocyte fate by interferon-gamma. Cytokine Growth Factor Rev. 22(1):35-43. Review.
Mitchell, K. A., Wilson, S. R. and Elferink, C. J. (2010) The activated aryl hydrocarbon receptor synergizes mitogen-induced murine liver hyperplasia. Toxicology 276(2):103-9.
Mitchell, K. A. and Elferink, C. J. (2009) Timing is everything: consequences of transient and sustained AhR activity. Biochem. Pharmacol. 77(6):947-56. Review.
Mitchell, K. A., Lockhart, C. A., Huang G. and Elferink, C. J. (2006) Sustained Ah receptor activity attenuates liver regeneration. Mol. Pharmacol. 70(1): 163-70.
Park, K. T., Mitchell, K. A., Huang, G. and Elferink, C. J. (2005) The Ah receptor predisposes hepatocytes to Fas-mediated apoptosis. Mol. Pharmacol. 67(3): 612-22.
Mitchell, K. A. and Lawrence, B. P. (2003) T cell receptor transgenic mice provide novel insights into understanding cellular targets of TCDD: Suppression of antibody production, but not the response of CD8+ T cells, during infection with influenza virus. Toxicol. Appl. Pharmacol. 192(3): 275-86.
Mitchell, K. A. and Lawrence, B. P. (2003) Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) renders influenza virus-specific CD8+ T cells hyporesponsive to antigen. Toxicol. Sci. 74(1): 74-84.
Jerrells, T. R., Mitchell, K., Pavlik, J., Jerrells, J. and Hoerman, D. (2002) Influence of ethanol consumption on experimental viral hepatitis. Alcohol. Clin. Exp. Res. 26(11): 1734-46.
Warren, T. K., Mitchell, K. A. and Lawrence, B. P. (2000) Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) suppresses the humoral and cell-mediated immune responses to influenza A virus without affecting cytolytic activity in the lung. Toxicol. Sci. 56(1): 114-123.
Jerrells, T. R., Sibley, D. A., Slukvin, I. I. and Mitchell, K. A. (1998) Effects of ethanol consumption on mucosal and systemic T-cell-dependent immune responses to pathogenic microorganisms. Alcohol. Clin. Exp. Res. 22(5 Sup): 212S-215S.