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Kevin Pruitt, Ph.D.
Assistant Professor
Ph.D., 2001, University of North Carolina at Chapel Hill
Department of Molecular and Cellular Physiology
LSU Health Sciences Center
1501 Kings Highway
Shreveport, LA 71130
Phone:
318-675-6033
Fax: 318-675-7393
E-mail:
kpruit@lsuhsc.edu |
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Biography
Dr. Kevin Pruitt began his formal education at the University of Texas at Austin where he received a B.S. degree in Chemical Engineering (1995). Afterwards, he pursued post-baccalaureate research training in the biological sciences at Los Alamos National Laboratory with Dr. Babetta Marrone, where his interest in the mysteries of the chromosome first germinated. At the University of North Carolina at Chapel Hill, under the direction of Dr. Channing J. Der, Dr. Pruitt earned his Doctorate degree in Pharmacology (2001). Dr. Pruitt’s interest in epigenetics blossomed during a short stint of postdoctoral training with Howard Hughes investigator Dr. Yi Zhang, also a member of the Lineberger Cancer Center at UNC. Subsequently, Dr. Pruitt completed postdoctoral training under the direction of Dr. Stephen Baylin at the Johns Hopkins University School of Medicine in the Department of Oncology (2006). There, Dr. Pruitt’s interest in cancer epigenetics grew rapidly and culminated in a recent publication selected as a Faculty of 1000 “Must Read”.
Dr. Pruitt has received numerous awards throughout his research career, some of which include the Hoechst-Celanese Corporation Research Scholarship Award, the Graduate School Excellence Award, the Merck-UNCF Graduate Science Research Dissertation Fellowship, and the Eli Lilly AACR Scholar in Training Award. Of note, Dr. Pruitt was also a National Science Foundation pre-doctoral fellow and an American Cancer Society postdoctoral fellow during his formal training. Currently, Dr. Pruitt serves as an Ad-hoc reviewer for the journals “Cancer Research” and “Molecular Cancer Research”. Dr. Pruitt’s long-term research interests include understanding the role of sirtuin proteins in cancer biology and epigenetic silencing, the focus of his research laboratory at the LSU Health Sciences Center in Shreveport. |
Research
In recent years, the increasing interest in Sirtuin protein biology has been astounding. The most prominent human family member, SIRT1, has received considerable attention because of its link with human metabolism, aging and cancer. My colleagues and I have shown that SIRT1 plays a key role in the epigenetic silencing of several tumor suppressor genes (TSG) and profoundly influences Wnt/ b -catenin signaling in cancer cells. The long-term focus of our laboratory involves defining the signaling pathways upstream and downstream of SIRT1 and characterizing the role that each plays in aberrant epigenetic regulation of gene silencing. The first major focus of our group involves delineating the upstream signals regulating SIRT1 activity (1) and characterizing their impact on epigenetic modifications. Second, we are interested in identifying non-histone targets that are positively (2) and negatively (3) regulated by SIRT1 and understanding the role that each plays in human disease. Finally, our group is interested in defining the mechanism by which SIRT1 leads to TSG silencing (4) and characterizing the impact this has on cellular transformation. |
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Selected Publications
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Ohm JE, McGarvey KM, Yu X, Cheng L, Schuebel KE, Cope L, Mohammad HP, Chen W, Daniel VC, Yu W, Berman DM, Jenuwein T, Pruitt K, Sharkis SJ, Watkins DN, Herman JG, Baylin SB.
A stem cell-like chromatin pattern may predispose tumor suppressor genes to DNA hypermethylation and heritable silencing. Nat Genet. 2007 Feb;39(2):237-42. Epub 2007 Jan 9.
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Zinn RL, Pruitt K, Eguchi S, Baylin SB, Herman JG.
hTERT is expressed in cancer cell lines despite promoter DNA methylation by preservation of unmethylated DNA and active chromatin around the transcription start site. Cancer Res. 2007 Jan 1;67(1):194-201. |
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Pruitt K, Zinn RL, Ohm JE, McGarvey KM, Kang SH, Watkins DN, Herman JG, Baylin SB.
Inhibition of SIRT1 reactivates silenced cancer genes without loss of promoter DNA hypermethylation. PLoS Genet. 2006 Mar;2(3):e40. Epub 2006 Mar 31. |
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Pruitt K, Ulku AS, Frantz K, Rojas RJ, Muniz-Medina VM, Rangnekar VM, Der CJ, Shields JM.
Ras-mediated loss of the pro-apoptotic response protein Par-4 is mediated by DNA hypermethylation through Raf-independent and Raf-dependent signaling cascades in epithelial cells. J Biol Chem. 2005 Jun 17;280(24):23363-70. Epub 2005 Apr 14. |
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Pruitt K, Pruitt WM, Bilter GK, Westwick JK, Der CJ.
Raf-independent deregulation of p38 and JNK mitogen-activated protein kinases are critical for Ras transformation.
J Biol Chem. 2002 Aug 30;277(35):31808-17. Epub 2002 Jun 24. |
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Shields JM, Mehta H, Pruitt K, Der CJ.
Opposing roles of the extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in Ras-mediated downregulation of tropomyosin.
Mol Cell Biol. 2002 Apr;22(7):2304-17. |
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Pruitt K, Der CJ.
Ras and Rho regulation of the cell cycle and oncogenesis.
Cancer Lett. 2001 Sep 28;171(1):1-10. Review. |
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For a complete list of publications by Kevin Pruitt in PubMed click here . |
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