BACKROUND:
Undergraduate: University
of North Carolina, Chapel Hill, NC, B.S. in Biology (Chemistry, minor),
1999.
RESEARCH INTERESTS: Effect of PPAR ligands on MAPK signaling
RESEARCH SUMMARY
Peroxisome proliferator activated receptors
(PPARs: a,
g,
d)
are nuclear hormone receptors that function as ligand-activated transcription
factors regulating lipid metabolism and homeostasis. Genes regulated by
PPARs have crucial roles in lipid metabolism, cellular differentiation,
glucose homeostasis, eicosanoid signaling, and inflammation. These receptors
have thus become an attractive target in the treatment of hyperlipidemia,
noninsulin-dependent diabetes, coronary artery disease, inflammation, and
possibly cancer prompting the development of synthetic PPAR agonists by
the pharmaceutical industry. The efficacy of PPAR ligands in modulating
lipid homeostasis has been largely attributed to their ability to modulate
gene transcription in a PPAR-dependent manner. However, recent studies
have shown that PPAR agonists exert PPAR-independent or 'non-genomic' effects
as they activate members of the mitogen-activated protein kinase (MAPK)
family at times too rapid to account for new protein synthesis. MAPKs alone
can mediate some of the effects of PPAR agonists; thus, kinase activation
by PPAR ligands could play an important role in the mechanism of action
of these compounds. Yet, few studies have investigated how PPAR agonists
stimulate MAPKs. The focus of my research is thus to characterize the mechanism(s)
responsible for PPAR ligand-dependent MAPK activation.
AWARDS
The Susan G. Komen Breast Cancer Foundation
Dissertation Research Award
Burroughs Wellcome Graduate Student
Scholar Award