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Kristen A. Mitchell |
Assistant Professor, Department of Biological Sciences |
| Department: |
Biological Sciences |
| Year arrived at BSU: |
2008 |
| Mailing Address: |
Department of Biology
Boise State
University
Boise, ID 83725-1515 |
| Office Location: |
Science/Nursing 105A |
| Office Number: |
208-426-4620 |
| Office Fax: |
208-426-4267 |
| E-Mail Address: |
kristenmitchell@boisestate.edu |
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ACADEMIC DEGREES
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B.S., Idaho State University, Microbiology, 1995
- Ph.D., Washington State University, Pharmacology/Toxicology, 2003
- Postdoctoral Fellow, University of Texas Medical Branch, Molecular Pharmacology, 2003-07
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TEACHING
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- Boise State University
BIOL 497/597 Toxicology
ZOOL 401/501 Human Physiology
- San Jacinto College, Houston, TX
BIOL 2401 Human Anatomy and Physiology I
BIOL 2402 Human Anatomy and Physiology II
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RESEARCH INTERESTS
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- Mitchell, K. A., Lockhart, C. A. and Elferink, C. J. (200X) p21Cip1 is required for Ah receptor-mediated suppression of liver regeneration. (in preparation)
- Mitchell, K. A. and Elferink, C. J. (200X) The long and the short of it: Consequences of transient and sustained Ah receptor activation. (under review)
- Mitchell, K. A., Wilson, S. R. and Elferink, C. J. (200X) Synergy between aryl hydrocarbon receptor and constitutive androstane receptor activation promotes murine liver hyperplasia. (under 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-tetrachloro-dibenzo-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.
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