|School||University of California, San Diego|
|Address||9500 Gilman Drive #0722|
CA La Jolla 92093
|Ph.D.||University of Iowa|
|B.S.||University of Minnesota|
As a large branch of drug-processing genes that compose several supergene families, UDP-glucuronosyltransferase (UGT) genes possess divergent regulatory properties that can be attributed to inherited genetic variations, developmental stages, transcription factors, co-factors, repressors, or environmental stimuli. Each component of this regulatory network plays an important role in controlling functional properties of these genes, thus affecting the body's ability to glucuronidate and eliminate drugs and endogenous and environmental toxicants. By applying mouse genetic techniques to generate mice humanized with the UGT1 locus, we model complex signaling and gene regulatory events that ultimately determine the delicate balance between homeostasis and disease.
Our current projects are as follows:
- We discovered that UGT1A is indispensable to maintain and sustain p53 activation in stress-induced colon epithelial cells, thus impacting p53-mediated apoptosis and colon tumor suppression; further work is designed to uncover the molecular mechanism underlying UGT1A-directed modulation of cytoplasmic p53 levels.
- By applying functional genomic approaches and employing chromatin pull-down and deep sequencing (CHIP-seq) and RNA-sequencing, we are studying the importance of the recruitment of the nuclear receptor co-repressor I (NCOR1) and resulting histone-modification dynamics on controlling the suppression of UGT1A expression.
- We are creating novel animal models in the humanized UGT1 background to examine the effect of clinically relevant genetic variants of the UGT1A1 gene on the onset of hyperbilirubinemia and bilirubin-induced neurological dysfunction owing to the fact that UGT1A1 is the sole bilirubin-metabolizing enzyme.
- Part of our research focus is to understand how environmental toxicants exert their adverse effects on health. We have recently demonstrated that the antibacterial agent triclosan is a liver tumor promoter. Experiments are underway to investigate how the involvement of inflammatory cytokines and what relevant oncogenic pathways contribute to TCS-induced tumorigenesis.
Signal Transduction, Gene Regulation, Carcinogenesis
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