BIOGRAPHY

Dr. Maureen Shuh is an Associate Professor in the Division of Basic Pharmaceutical Sciences in the College of Pharmacy.  Dr. Shuh earned her Bachelor of Arts (B.A.) degree in the Department of Microbiology and Immunology in 1986 from the University of California at Berkeley and her Doctor of Philosophy (Ph.D.) in the Program in Molecular Biology, Cell Biology and Biochemistry in the Department of Biology in 1996 from Brown University, Providence, RI.  Her doctoral project focused on the V(D)J DNA recombination mechanisms that give rise to immunoglobulin/antibody diversity.  In 1983-1986, between her undergraduate and graduate degrees, Dr. Shuh was a Research Associate at Chiron Corporation (currently Novartis Pharmaceuticals), Emeryville, CA, one of the first genetic engineering companies in the San Francisco Bay Area, where she worked on the vaccine project for the newly discovered AIDS virus (HIV).   After obtaining her graduate degree, Dr. Shuh was a post-doctoral fellow from 1996-2000 at the National Cancer Institute (NCI) in Frederick, MD, where she studied HLTV-I and its transformation mechanisms.  Dr. Shuh joined the College of Pharmacy faculty in 2008.

Prior to joining the Xavier faculty, Dr. Shuh was an Assistant Professor, then an Associate Professor, in the Department of Biological Sciences at Loyola University New Orleans where she earned the Faculty Senate Excellence awards in teaching and advising.  In the College of Pharmacy, Dr. Shuh teaches Biomedical Immunology for first-year pharmacy students and Basic and Clinical Nutrition for third-year pharmacy students.  Dr. Shuh is a member of the American Association for the Advancement of Science (AAAS), American Association for Cancer Research (AACR), American Society for Microbiology (ASM), South Central Branch of the American Society for Microbiology (SCB/ASM), American Society for Biochemistry and Molecular Biology (ASBMB), and American Association for University Professors.  Her research is funded by the National Institutes of Health (NIH), the Louisiana Board of Regents (LaBoR), the Cancer Association of Greater New Orleans (CAGNO), and the Louisiana Cancer Research Consortium (LCRC).

RESEARCH INTEREST

Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of two human diseases, adult T cell leukemia (ATL) and tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM).   The viral genome contains a 3’ region which encodes at least five overlapping reading frames (ORFs I-V).  The gene product of ORF IV is a 40 kDa, 353 amino acid, phosphorylated protein known as Tax, the transforming protein of HTLV-1.  The focus of our current and future research is the molecular mechanisms of Tax leukemogenesis.

Tax activates viral gene expression via the long terminal repeat (LTR) and host genes by modulating the activities of two promoters, the nuclear factor-kB (NF-kB) promoter and the serum response element (SRE).  Our experiments focus on determining the mechanisms by which Tax activates transcription of host genes from the SRE.  During normal stimulation of cell proliferation by growth factors, two proteins, the serum response factor (SRF) and a ternary complex factor (TCF), bind directly to the SRE.  Proteins that function as TCFs are members of the Ets transcription factor family, Elk-1, Sap-1, and Sap-2.  Tax has been shown in published reports to interact directly with SRF and TCF and to recruit the histone acetyltransferases CREB binding protein (CBP) and p300/CBP-associated factor (P/CAF) to the SRE/SRF/TCF/Tax complex.  We are currently examining Tax regulation of the SRF pathway in four areas:  (1.) the direct interaction of Tax and SRE-associated proteins to activate transcription, (2.) the elucidation of the secondary and tertiary structure of Tax, (3.) the role of Tax in enhancing the activity of the mitogen activated protein kinase (MAPK) signal transduction pathway which is required for TCF activation, and (4.) the role of Tax in regulating inhibitors of the SRF pathway.   Results from our experiments will enable us to test our hypothesis that Tax regulation of the SRF pathway initiates T cell transformation by HTLV-1.  The results of our experiments will allow us to construct Tax mutants in a molecular clone of the virus and to determine the function of Tax in the context of the whole virus and its ability to transform T cells due to Tax up-regulation of SRF-mediated transcription.

LINKS

http://www.lcrc.info/research/researchers/facs.htm