M. Tino Unlap | OMICS International
ISSN: 2155-952X

Journal of Biotechnology & Biomaterials
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M. Tino Unlap

 Departments of Clinical and Diagnostic Sciences, Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294


 Dr. Unlap received his PhD in Biochemistry/Molecular Biology from Kansas State University followed by postdoctoral trainings in Hematology/Oncology and Behavioral Neurobiology at the UAB Cancer Center and Behavioral Neurobiology where he studied the roles that immediate early genes play in the pathogenesis of malignancy and neuronal degeneration. From 2000-2007 he was a faculty member in the Division of Nephrology but left for a faculty appointment at the Tulane School of Medicine. Dr. Unlap returned to UAB in the spring of 2008 to help start the biotech program where he now serves as a faculty member.
Since 1995 Dr. Unlap has mentored over 200 postdocs, graduate, undergraduate and high school students and represent Science and Technology Honors, Experiential Learning Scholars, Early Medical School Acceptance, Biology Honors, Chemistry Honors, Summer In Biomedical Sciences, NIH/Drew University Summer Research, Louis-Stokes Alliance for Minority Participation, Project SEED, MHRC Summer Interns and the UAB Community Outreach Development (CORD) Summer Research Programs. His research interests include cancer and Parkinson’s disease drug discovery, wound healing, the genetic basis of salt sensitive hypertension and Latent TB detection and eradication
Research Interest

 My laboratory is studying the role that oxidative stress plays in the pathogenesis of hypertension.  Studies have shown that the adverse effects of oxidative stress are mediated through reactive oxygen species which include  superoxide anion (O2.-), hydrogen peroxide (H2O2), hydroxyl radical (OH.-) and peroxynitrite (ONOO-), which exert a variety of effects in the renal vasculature including dysregulation of cytosolic calcium homeostasis, elevation of intracellular Na+ and Ca2+ and induction of membrane depolarization.  Because the Na+/Ca2+ exchanger plays a crucial role in maintaining cytosolic calcium homeostasis, we hypothesize that elevation of intracellular Na+ levels which leads to membrane depolarization and increased Ca2+ influx through the Na+/Ca2+ exchanger, an effect which is significantly greater in renal vasculature of the Salt Sensitive Dahl rat. Studies in my laboratory is are testing this hypothesis in preglomerualr vascular smooth muscle cells of Salt Sensitive and Salt Resistant Dahl rats and, for mechanistic studies, in Opossum kidney (OK) cells stably expressing RiNCX and SfNCX,  two Na+/Ca2+ exchanger isoforms that we previously cloned from renal vasculatures of the Salt Resistant and Salt Sensitive Dahl rats, respectively.


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