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The Department of Dermatology deals with all aspects of the biology and diseases of the skin.

Department of Dermatology

Qinghong Zhang, Ph.D.

Dr. Qinghong Zhang

Assistant Professor
Department of Dermatology
Phone: (303) 724-4051                                                   

Research Interests: 

Transcriptional regulation governs a broad spectrum of cellular activities: cell cycle progression, cell migration, apoptosis, or metabolism. We are interested in elucidating the molecular mechanisms underlying transcriptional regulation in response to physiological and pathological signals. Particularly, our research over the past decade has focused on CtBP, a transcriptional co-repressor, and has uncovered a unique function of this protein as a redox-sensor in transcription control. This function allows cells to couple the metabolic status with gene expression. Furthermore, we demonstrate that CtBP is subjected to post-translation modifications in response to cellular stress and, consequently, triggering apoptosis independent of p53. Both aspects of our research have important therapeutic implications in human diseases. The ultimate and long-term goal of my lab is to develop drugs against metabolic disorders and cancers based upon molecular details as revealed by basic research.

Dr. Zhang's lab 

Recent Selected Publications:


Zhang, Q., D. W. Piston, and R. H. Goodman. Regulation of corepressor function by nuclear NADH. Science. 2002 295:1895-7. 

Zhang, Q. *, Y. Yoshimatsu, J. Hildebrand, S. M. Frisch, and R. H. Goodman. Homeodomain interacting protein kinase 2 promotes apoptosis by downregulating the transcriptional corepressor CtBP. Cell  2003 115:177-86.   *corresponding author

Zhang, Q. *, S. Y. Wang, A. C. Nottke, J. V. Rocheleau, D. W. Piston, and R. H. Goodman*. Redox sensor CtBP mediates hypoxia-induced tumor cell migration. Proc. Natl. Acad. Sci. U S A. 2006 103:9029-33. *corresponding author

Wang, S. Y., M. Iordanov, and Q. Zhang. C-Jun NH2-terminal kinase promotes apoptosis by down-regulating the transcriptional co-repressor CtBP. J. Biol. Chem. 2006 281:34810-5        

Zhang, Q. *, S. Y. Wang, C. Fleuriel, D. Leprince, J. V. Rocheleau, D. W. Piston, and R. H. Goodman*. Metabolic regulation of SIRT1 transcription via a HIC1:CtBP co-repressor complex. Proc. Natl. Acad. Sci. U S A. 2007. 104:829-33  *corresponding author

Deng, Y., J. Liu, G. Han, S. L. Lu, S. Y. Wang, S. Malkoski, A. C. Tan, C. Deng, X. J. Wang, and Q. Zhang. Redox-dependent Brca1 transcription by an NADH-sensor CtBP1. Oncogene 2010  Dec 16;29(50):6603-8. PMID: 20818429

Deng, H., J. Liu, Y. Deng, G. Han, S. Shellman, Y. G., Robinson, S., Tentler, J., Robinson, W., Norris, D. A., X. J. Wang, and Q. Zhang. CtBP1 is expressed in melanoma and represses the transcription of p16INK4a and Brca1. Journal of Investigative Dermatology 2013 Jan 10. PMID:23303449

Han, G., L. Bian, F. Li, A. Cotrim, D. Wang, J. B. Lu, Y. Deng, G. Bird, A. Sowers, J. Mitchell, J. S. Gutkind, R. Zhao, D. Raben, P. ten Dijke, Y. Refaeli, Q. Zhang* and X. J. Wang*. Preventive and therapeutic effects of Smad7 on radiation-induced oral mucositis. Nature Medicine 2013 Mar 10. doi: 10.1038/nm.3118. PMID: 23475202 *corresponding author