Aloysius J. Klingelhutz, Ph.D.
Ph.D., University of Wisconsin-Madison (Genetics), 1991 |
Associate Professor of Microbiology Campus address: 2202 MERF Mailing address: 375 Newton Rd. 2202 Medical Education and Biomedical Research Facility Iowa City, IA 52242 Phone: 319-335-7788 Email: |
Genetic factors involved in aging and cancer
In the broadest sense, my goal is to understand the biology and genetics of human cancer and aging. It is hoped that the research in my laboratory will lead to better methods to prevent, diagnose, and treat human disease. One of my primary interests is in how epithelial cells become immortal and subsequently malignant after infection with human papillomavirus (HPV). We are also studying how telomere loss and other factors are involved in induction of cellular senescence and aging. Specific areas of research are the following: 1) Examining the regulation of cellular genes by HPV E6 and E7 during the process of infection and transformation; 2) Developing cell-specific modified RNA aptamers for diagnosis and treatment of HPV associated cancers; 3) Defining how telomere loss and telomerase dysfunction leads to cell aging and transformation; 4) Determining the mechanism and consequences of oxidative stress induction during cell senescence.
Additional information
UI Carver College of Medicine Interview
UI Interdisciplinary Graduate Program in Molecular Biology
UI Medical Scientist Training Program
Recent publications
Agarwal, S., Loh, Y.H., McLoughlin, E.M., Huang, J., Park, I.H., Miller, J.D., dos Reis, R.M., Okuka, M., Huo, H., Loewer, S., Goldman, F.D., Keefe, D.L., Klingelhutz, A.J., Liu, L., Daley, G.Q. Telomere elongation in dyskeratosis congenita induced pluripotent stem cells. Nature 464:292-296, 2010. PMC Journal-In Process.
Gourronc, F.A., Robertson, M.M., Herrig, A.K., Lansdorp, P.M., Goldman, F.D., and Klingelhutz, A.J. Proliferative defects in dyskeratosis congenita skin keratinocytes are corrected by expression of the telomerase reverse transcriptase, TERT, or by activation of endogenous telomerase through expression of papillomavirus E6/E7 or the telomerase RNA component, TERC. J. Exper. Dermatol. 19:279-288, 2010. PMC2852488.
Spanos, W.C., Hoover, A., Harris, G.F., Wu, S., Strand, G.L., Anderson, M.E., Klingelhutz, A.J., Hendriks, W., Bossler, A.D., and Lee, J.H. The PDZ binding motif of human papillomavirus type 16 E6 induces PTPN13 loss, which allows anchorage –independent growth and synergizes with ras for invasive growth. J. Virology, 82:2493-2500, 2008, PMC2258903.
Westin, E.R., Chavez, E., Lee, K.M., Gourronc, F.A., Riley, S., Lansdorp, P.M., Goldman, F.D., and Klingelhutz, A.J. Telomere restoration and extension of proliferative lifespan in autosomal dominant dyskeratosis congenita fibroblasts. Aging Cell, 6:383-394, 2007, PMC2225626.
James, M.A., Lee, J.H., and Klingelhutz, A.J., Human papillomavirus type 16 E6 activates NFkB, induces cIAP-2 expression, and protects against apoptosis in a PDZ binding motif-dependent manner. J. Virol., 80:5301-5307, 2006, PMC1472131.
James, M.A., Lee, J.H., and Klingelhutz, A.J., HPV16-E6 associated hTERT promoter acetylation is E6AP dependent, increased in later passage cells, and enhanced by loss of p300. Int. J. Cancer, 119:1878-1885, 2006, PMC2223064.