Department of Molecular and Cellular Biology
Baylor College of Medicine
Houston, Texas, United States
Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas, United States


PhD from Georgetown University
Post-Doctoral Fellowship at Yale University
Molecular Biophysics and Biochemistry

Honors & Awards

USC Mellon Mentoring Award
Outstanding Graduate Student Teaching Award
Zorbac Award for outstanding Ph.D. thesis

Professional Interests

  • Transcription Factors
  • Oncogenic Transformation
  • PTEN
  • TATA-binding protein
  • Maf1
  • Graduate Student Education

Professional Statement

The goal of our research is to delineate the regulation and roles of transcription factors in oncogenic transformation. One major area of investigation is to define key downstream targets of PTEN that confer its ability to negatively regulate metabolism and oncogenesis. We have so far identified two large classes of genes transcribed by RNA polymerases (pols) I and III that are repressed by PTEN through its ability to regulate PI3K signaling. The products of these genes, which transcribe rRNAs, tRNAs and a variety of untranslated RNAs, constitute 80% of all cellular RNA. Furthermore, we showed that PTEN-mediated repression of RNA pol III-dependent transcription is required for oncogenic transformation.

In our second major area of research, we have defined an unexpected role for the central transcription initiation factor, TATA-binding protein (TBP) in promoting oncogenesis, and extensively identified intriguing and unanticipated properties of growth factor receptors and signaling molecules that regulate its expression. We demonstrated that enhanced expression of TBP is associated with human colon cancer. Further exploring the mechanisms that regulate cellular TBP concentrations, and subsequently, the rate of RNA pol I- and III-dependent transcription, we discovered a new protein, Maf1. Maf1 directly represses transcription from both RNA pol II- and III-dependent genes, but not RNA pol I genes, making it a unique transcription factor. We have recently made the interesting discovery that Maf1 expression is regulated by PTEN and that altered Maf1 expression results in changes in the expression of genes involved in lipid metabolism. Thus, we are now in a highly unique position to address a central question in the field that will define Maf1 as a pivotal link between metabolism and cancer. Our studies over the years have made significant, and often unexpected, contributions to our understanding of transcription regulation, cellular signaling pathways, and oncogenesis.


American Association for Cancer Research
American Society for Microbiology
American Society of Molecular Biology and Biochemistry


Maf1, a novel regulator of the TATA-binding protein
- #R01 CA74138
National Cancer Institute
This grant is identifying the molecular events by which Maf1 negatively represses transcription. We will investigate the hypothesis that Maf1 associates with the mediator CDK8 subcomplex to antagonize its ability to induce gene expression and oncogenic transformation.
Novel targets that are deregulated by the loss of PTEN
- #R01 CA108614
National Cancer Institute
Based on our new results that Maf1 is regulated by PTEN and PI3K signaling, these studies will define Maf1 as a pivotal link between metabolism and cancer, and elucidate a novel role for this transcription repressor in regulating lipid metabolism.

Intellectual Property

Compositions and methods for alleviating stress, anxiety and seizure activity
Co Inventors: Gee KW, Bolger MB, Brinton RE and McEwen BS