Mike Kemp
 Ph.D.
Department of PHARMACOLOGY & TOXICOLOGY
Wright State University
United States of America
Biography
Education History: ​Postdoctoral Training ​​(Mar 2016 - April 2017) Wright State University Department of Pharmacology & Toxicology Advisor: Jeffrey B. Travers, M.D., Ph.D. Postdoctoral Training (Sept 2006- Sept 2011) University of North Carolina School of Medicine, Department of Biochemistry & Biophysics Advisor: Aziz Sancar, M.D., Ph.D. Ph.D. in Biomedical Sciences (Biochemistry/Molecular Biology) (Sept 2001 - Aug 2006) Wright State University, Department of Biochemistry and Molecular Biology Dissertation: “Regulation of DNA Replication Initiation by Histone Acetylation and the DNA Unwinding Element Binding Protein DUE-B” Advisor: Michael Leffak, Ph.D. B.S. in Biological Sciences (Sept 1995 - June 1999) Wright State University, Department of Biological Sciences
Research Interest
His research interests lie in understanding how human cells maintain the integrity of their genomic DNA, particularly in response to environmental genotoxins such as ultraviolet (UV) light. He utilize a variety of methods and techniques in biochemistry, molecular biology, cell biology, and genetics to approach these issues. Ultraviolet (UV) light and other environmental carcinogens induce the formation of adducts on genomic DNA. This DNA damage is potentially mutagenic or toxic, and thus human cells go to great lengths to maintain the integrity of their genetic information in response such stress. A variety of biochemical processes, including DNA repair and DNA damage checkpoint signaling, help cells to cope with this DNA damage by allowing cells time to remove DNA lesions and minimizing replication errors. Abnormalities in DDR activities are associated with a number of human diseases, including cancer and aging. My laboratory is interested in identifying and characterizing the mechanisms of the human DDR, particularly in the context of human skin. His current projects are focused on understanding the ways in which the ATR (ataxia telangiectasia and rad3-related) protein kinase controls various aspects of the DNA damage response in human skin. He is particularly interested in understanding how ATR kinase function may become de-regulated as people age, which is an important concern given that the majority of non-melanoma skin cancers are found in people over the age of 60. I am currently investigating a role for insulin-like growth factor (IGF-1) in this regulation because there is significant data showing that IGF-1 signaling is altered in the skin of geriatric individuals in comparison to young adults. Additional research projects are aimed at describing the cellular functions of a class of small DNA molecules, termed sedDNAs (for small, excised, damage-containing DNA oligonucleotides), that are generated through a dual incision process by the nucleotide excision repair system in response to environmental agents and chemicals that generate bulky adducts on DNA, such as ultraviolet (UV) light from the sun. Normal, incidental exposures to sunlight lead to the production of hundreds of thousands of sedDNAs in every skin cell. The fate of these UV photoproduct-containing sedDNAs is completely unknown, but they are expected to influence DNA metabolism and cell physiology. His group is particularly interested in determining whether UV-sedDNAs contribute to the photosensitivity that is associated with autoimmune disorders, such as lupus.
Publications
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Canturk F, Karaman M, Selby CP, Kemp MG, Kulaksiz-Erkmen G, Hu J, Li W, Lindsey-Boltz LA, and Sancar A. (2016). Nucleotide excision repair by dual incisions in plants. Proc Natl Acad Sci USA. 113(17): 4706-10.
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Kemp MG, Spandau DF, Simman R, Travers JB. (2017). Insulin-like Growth Factor-1 Receptor Signaling is Required for Optimal ATR-CHK1 Kinase Signaling in Ultraviolet B (UVB)-irradiated Human Keratinocytes. J Biol Chem. 292(4): 1231-9.
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Kemp MG. (2017) DNA damage-induced ATR kinase activation in non-replicating cells is regulated by the XPB subunit of transcription factor II-H (TFIIH). J Biol Chem. 292(3): 12424-35.