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Kristen A. Mitchell, Ph.D.

Associate Professor

Year arrived at BSU: 2008

Mailing Address:
Department of Biological Sciences
1910 University Drive
Boise State University
Boise, ID 83725-1515

Office Location: Science Building, Room 102B
Office Number: 208-426-4620
Office Fax: 208-426-1040
E-Mail Address: kristenmitchell@boisestate.edu

ACADEMIC DEGREES

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

TEACHING

  • ZOOL 401/501 Human Physiology
  • BIOL 440/540 General and Molecular Toxicology
  • BIOL 205 Introductory Microbiology
  • BIOL 301 Cell Biology

RESEARCH INTERESTS

Pharmacology of the aryl hydrocarbon receptor (AhR) and toxicology of AhR ligands during liver regeneration and fibrosis.

PUBLICATIONS

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.journalinflammation.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.