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DepartmentOffice of the Vice President for Research Medicine/ Microbiology, Immunology & Molecular Genetics (Physiology) (South Texas Veterans Health Care System)
Clark, Robert A., M.D.
Dr. Clark has over 30 years of experience in basic and translational research relevant to human diseases, with a major focus on mechanisms of the inflammatory response and oxidative stress, as well as the cell biology and biochemistry of human phagocytic cells. Dr. Clark’s lab has contributed to the fundamental understanding of the generation of reactive oxygen species by the phagocyte NADPH oxidase system, the biological roles of these products, the transcriptional and post-translational regulation of NADPH axidase components, and the genetics and biochemistry of NADPH oxidase deficiency. In recent years they have turned our attention to the structure, function, and physiologic roles of several novel non-myeloid members of the NADPH oxidase (NOX) gene family and the involvement of these oxidase in disease pathogenesis. Dr. Clark has also been active as a member of a collaborative team of investigators examining host determinants of HIV-1 susceptibility, disease progression, and response to therapy through in-depth analysis of multiple large cohorts of HIV-1 infected subjects.
M.D., Medicine at Columbia University, New York, NY
Dr. Robert Clark’s lab carries out basic and translational research relevant to human diseases, with a major focus on mechanisms of the inflammatory response and oxidative stress, as well as the cell biology and biochemistry of human phagocytic cells. We have contributed to fundamental understanding of the generation of reactive oxygen species (ROS) by the phagocyte NADPH oxidase system, the biological roles of these products, and the genetics and biochemistry of NADPH oxidase deficiency.
In recent years, we have turned our attention to the structure, function, and physiologic roles of several novel non-myeloid members of the NADPH oxidase (NOX) gene family, focusing particularly on the involvement of these oxidases in disease pathogenesis and the transcriptional regulation of genes that are relevant to the biology of aging. Our recent studies include mechanistic work on neurodegenerative disorders, especially Parkinson’s disease.
Le T, Wright EJ, Smith DM, He W, Catano G, Okulicz JF, Young JA, Clark RA, Richman DD, Little SJ, Ahuja SK. Enhanced CD4+ T-cell recovery with earlier HIV-1 antiretroviral therapy. N Engl J Med 368(3):218-230, 2013.
Imam SZ, Trickler W, Kimura S, Binienda ZK, Paule MG, Slikker Jr. W, Li S, Clark RA, Ali SF. Neuroprotective efficacy of a new brain-penetrating c-Abl inhibitor in a murine Parkinson’s disease model. PLoS ONE 8(5): e65129, 2013. doi:10.1371/journal.pone.0065129.
Okulicz JF, Le TD, Agan BK, Camargo JF, Landrum ML, Wright E, Dolan ML, Ganesan A, Ferguson TM, Smith DM, Richman DD, Little SL, Clark RA, He W, Ahuja SK. Influence of the timing of antiretroviral therapy on the potential for normalization of immune status in human immunodeficiency virus 1-infected individuals. JAMA Intern Med 175(1):88-99, 2015.
de Figueiredo ASP, Salmon AB, Bruno F, Jimenez F, Martinez HG, Halade GV, Ahuja SS, Clark RA, DeFronzo RA, Abboud HE, El Jamali A. Nox2 mediates skeletal muscle insulin resistance induced by a high-fat diet. J Biol Chem 290(21):13427-13439, 2015.
He W, Jimenez F, Martinez H, Harper NL, Manoharan MS, Carrillo A, Ingale P, Liu YG, Ahuja SS, Clark RA, Rather CG, Ramirez DA, Andrews CP, Jacobs RL, Ahuja SK. Cockroach sensitization mitigates allergic rhinoconjunctivitis symptom severity in patients allergic to house dust mites and pollen. J Allergy Clin Immunol 136:658-666, 2015.
Gornalusse G, Mummidi S, Gaitan AA, Jimenez F, Ramsuran V, Picton A, Rogers K, Manoharan M, Avadhanam N, Murthy KK, Martinez H, Molano Murillo AM, Chykarenko ZA, Hutt R, Daskalakis D, Shostakovich-Koretskaya L, Karim SA, Martin JN, Deeks SG, Hecht F, Sinclair E, Clark RA, Okulicz J, Valentine FT, Martinson N, Tiemessen CT, Ndung’u T, Hunt PW, He W, Ahuja SK. Epigenetic mechanisms, T-cell activation, and CCR5 genetics interact to regulate T-cell expression of CCR5, the major HIV-1 coreceptor. Proc Natl Acad Sci USA 112:E4762-E4771, 2015.
Clark RA. Proton pathway paradox: Hv1 H+ channel sustains neutrophil Nox2 activity, yet suppresses HOCl formation. J Leukocyte Biol 99:1-3, 2016.