First name,Last name,Preferred title,Overview,Position,Department,Individual
James,Samuel,Regents Professor and Head,"Our laboratory works with the obligate intracellular bacterial pathogen, Coxiella burnetii, the etiologic agent of Q fever and a category B biothreat agent. The long-term goal of this research is to understand the molecular pathogenic mechanisms involved in the host-pathogen interaction. To accomplish this broad goal, project in the lab are designed to test the molecular mechanisms employed by both the host and pathogen. Current pathogen studies include 1) broad survey of proteins secreted via a type 4 secretion system (T4SS) followed by determination of essentiality of each substrate for virulence and detailed analysis of mechanism of host modulation 2) survey of essential virulence loci identified by specific mutant screens, and 3) definition of the relative virulence of phylogenetically distinct isolate groups.",Regents Professor and Head,Microbial Pathogenesis and Immunology,https://scholars.library.tamu.edu/vivo/display/n01c3216f
Van,Wilson,Professor,"My area of specialization is the molecular biology of papovaviruses, with a primary focus on how viral proteins modify the host cell environment. Recently, we determined that the viral replication proteins, E1 and E2, are post-translationally modified by addition of 1 or more SUMO moieties. Sumoylation is a widespread modification whose biological functions are only recently becoming understood. Studies are in progress to 1) determine the role of sumoylation in the viral life cycle, 2) evaluate the effect of sumoylation on the structure and activity of the E1 helicase, 3) understand the mechanism by which sumoylation influences E2 stability and transcriptional activity, and 4) determine how sumoylation is modulated by the viral E6 oncoprotein. In addition to the role of sumoylation in the viral life cycle, we are also exploring how sumoylation participates in normal keratinocyte differentiation. We have developed a keratinocyte cell line inducibly expressing a tagged SUMO moiety to facilitate proteomics studies of sumoylation changes and regulation during controlled differentiation.",Professor,Microbial Pathogenesis and Immunology,https://scholars.library.tamu.edu/vivo/display/n4837bbf9
Jianxun,Song,Professor,T cell biology
T cell-based immunotherapy
Cell metabolism,Professor,Microbial Pathogenesis and Immunology,https://scholars.library.tamu.edu/vivo/display/n5b9879a8
Jon,Skare,Regents Professor and Associate Head,"Jon Skare is Regents Professor and Associate Head of the Department of Microbial Pathogenesis and Immunology in the College of Medicine at Texas A&M University. He has been a faculty member at Texas A&M since 1996 and has led a research laboratory centered around the pathogenic mechanisms operative in Borrelia burgdorferi, the spirochetal bacterium that causes Lyme disease. He has published over 50 peer reviewed manuscript, reviews, and book chapters and been funded continuously by the NIH since 1999 with over $20 million dollars in total costs. Dr. Skare has trained ten graduate students, sixteen postdoctoral fellows, and numerous undergraduate students in his research group during his time at Texas A&M. The majority of his postdoctoral trainees and students have gone on to hold academic or industry positions in the medical sciences.
Research interests are focused on microbial pathogenesis with an emphasis in spirochetal infections, particularly Borrelia burgdorferi, the etiologic agent of Lyme disease. Broad training in the molecular biology, genetics, and biochemistry of prokaryotic systems is employed to answer research-related questions. Long-term interests in the lab are centered on understanding how B. burgdorferi promotes its pathogenic potential and persists in the disparate hosts it occupies in nature (e.g., both ticks and mammals). In this regard, the research program is aligned with: (i) regulatory pathways that contribute to the establishment of infection during the arthropod to mammalian transition; (ii) identifying and characterizing surface structures that contribute to the colonization and maintenance of infection via adherence mechanisms; and (iii) the ability of B. burgdorferi and relapsing fever Borrelia to persistently infect hosts in the face of a potent innate and adaptive immune response.",Professor and Associate Head,Microbial Pathogenesis and Immunology,https://scholars.library.tamu.edu/vivo/display/n638ae603