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  • Boyer, Thomas G
Dr Boyer

Contact

210-562-4151

boyer@uthscsa.edu

Programs

  • M.D./Ph.D. in South Texas Medical Scientist Training Program
  • M.S. in Personalized Molecular Medicine
  • Ph.D. in Integrated Biomedical Sciences
  • Cancer Biology
  • Cell Biology, Genetics, and Molecular Medicine

Departments & Divisions

  • Department of Molecular Medicine

Research

Research profile

Currently seeking M.S. & Ph.D. students

Thomas G. Boyer, Ph.D.

Professor

The unifying theme of our research program is to understand the function and regulation of the multiprotein Mediator of transcription, and further clarify how Mediator dysfunction as a consequence of mutation or misexpression of its constituent subunits contributes to human disease. Mediator is a conserved multisubunit signal-processor through which regulatory information conveyed by gene-specific transcription factors is transduced to RNA polymerase II. In this capacity, Mediator serves to channel regulatory signals from activator and repressor proteins to affect changes in gene expression programs that control diverse physiological processes, including cell growth and homeostasis, development, and differentiation. Structurally, Mediator is assembled from a set of 26 core subunits into three distinct modules termed “head”, “middle”, and “tail” that bind tightly to RNA Polymerase II. MED12, along with MED13, CDK8, and Cyclin C (CycC), comprise a fourth “kinase” module that resides in variable association with core Mediator. Notably, we and others have shown that Mediator kinase activity is required for nuclear transduction of signals instigated by multiple developmental and oncogenic pathways. Our primary research interest over the past several years has centered on the Mediator kinase module and its role as an endpoint in these fate-determining signal transduction pathways. In this regard, we aim understand how physiological cell signals that converge on the kinase module in Mediator inform proper development of the brain, uterus, prostate, and intestine. Further,  we seek to clarify how pathological dysregulation of these signals elicits X-linked intellectual disability and neurodegenerative disease, uterine leiomyomas, and prostate and colorectal cancers. We expect these studies to reveal important mechanistic insight concerning the function of Mediator in developmental gene control that might be leveraged to advantage in the development of molecularly targeted therapies across a range of human pathologies.

Related Diseases: Uterine leiomyomas, Colorectal and Prostate Cancers, X-linked intellectual disability and Alzheimer’s disease.

Techniques: Biochemistry, Molecular/Cell biology, human stem cell- and animal-based models .

  • Professional Background

    Education

    • 1990 - PhD - Biochemistry - State University of New York at Buffalo
    • 1983 - BS - Wildlife/Fisheries Management - Frostburg State University
    • 1983 - BS - Biology - Frostburg State University
    • Postdoctoral Fellowship - Biochemistry/Molecular Genetics - University of California, Los Angeles

    Appointments

    • 9/2010 - Professor - The University of Texas Health Science Center at San Antonio, Molecular Medicine, San Antonio
  • Instruction & Training

    • - Present, Membership on Supervising Committee, The University of Texas Health Science Center
    • 1/2014 - Present, Post-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
    • 9/2013 - Present, Basic Radiation Biology, The University of Texas Health Science Center
    • 12/2012 - Present, Post-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
    • 5/2012 - Present, Pre-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
    • 5/2011 - Present, Ph.D. Dissertations Directed, The University of Texas Health Science Center, San Antonio
    • 5/2011 - Present, Pre-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
    • 5/2009 - Present, Ph.D. Dissertations Directed, University of Texas Health Science Center
    • 5/2009 - Present, Pre-Doctoral Student Supervision, The University of Texas Health Science Center at San Antonio
    • 2/2009 - Present, Membership on Supervising Committee, The University of Texas Health Science Center
    • 9/2001 - Present, Colloquium in Mol Medi, The University of Texas Health Science Center
    • 9/2000 - Present, Mod Meth/Cell-mole Bio, The University of Texas Health Science Center
    • 9/2000 - Present, Mod Meth/Cell-mole Bio, The University of Texas Health Science Center
    • 9/1999 - Present, Adv Molecular Cell Bio, The University of Texas Health Science Center
  • Research & Grants

    The unifying theme of our research program is to understand the function and regulation of the multiprotein Mediator of transcription, and further clarify how Mediator dysfunction as a consequence of mutation or misexpression of its constituent subunits contributes to human disease. Mediator is a conserved multisubunit signal-processor through which regulatory information conveyed by gene-specific transcription factors is transduced to RNA polymerase II. In this capacity, Mediator serves to channel regulatory signals from activator and repressor proteins to affect changes in gene expression programs that control diverse physiological processes, including cell growth and homeostasis, development, and differentia

    Research profile

    Grants

    Federal

    Funding Agency NIH Title Hypovitaminosis D promotes MED12-associated genomic instability in uterine fibroids Status Active Period 8/2017 - 7/2022 Role Principal Investigator Grant Detail : Vitamin D3 signaling modulates the level of DNA damage, including that likely arising from R-loop induced replication stress, in MED12 mutation positive uterine fibroids. These findings provide sound support to investigate whether, and also how, low vitamin D3 levels, a known risk factor for uterine fibroid development, compound DNA damage accumulation and genetic instability found in MED12 mutant tumors. Funding Agency NIH/NICHD Title Molecular basis of MED12 in the pathogenesis of uterine fibroids Status Active Period 8/2017 - 4/2022 Role Principal Investigator Grant Detail The major goals are to establish the requirement, mechanism, and therapeutic implications of mutant MED12-mediated transcriptional reprogramming in uterine fibroid pathogenesis.

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