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Gerald S. Shadel |
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| Associate Professor of Pathology and Genetics |
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B.S. Chemistry, University of Nevada, Las Vegas, 1986
Ph.D. Biochemistry, Texas A&M University. 1991
Postdoctoral Fellow, Stanford University
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| Research Interests: | |
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Mitochondrial Genetics and Biogenesis
Mitochondrial Dysfunction in Human Disease and Aging
Mechanisms of mtDNA Transcription and Mitochondrial Translation
Signaling Pathways that Sense and Control Mitochondrial Function
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| Honors: | |
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* Amgen Outstanding Investigator Award, American Association for Investigative Pathology (ASIP), 2007
* Glenn AFAR, Breakthroughs in Gerontology (BIG) Award, 2006
* Damon Runyon-Walter Winchell Postdoctoral Fellow, 1992-1995
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| Current Research: | |
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| In
humans, as in most animal cells, genetic information is housed not
only in the nucleus, but also in mitochondria. Mitochondrial DNA
(mtDNA) encodes thirteen essential proteins of the oxidative
phosphorylation complexes as well as 22 tRNAs and 2 rRNAs required to
translate these thirteen mRNAs in the mitochondrial matrix. Mutations
in mtDNA cause maternally inherited neuromuscular disorders due to
declines in cellular energy metabolism. In addition, mtDNA mutations
accumulate in normal aging tissues, certain tumors, and have been
implicated in late-onset diseases such a Alzheimer's, Parkinson's,
and diabetes, indicating that the pathology of dysfunctional
mitochondria is only beginning to be unraveled. The research in my
laboratory is directed toward understanding the mechanism of gene
expression in human mitochondria and its impact on human aging and
disease. The ultimate goal is to understand the full impact of
dysfunctional mitochondrial gene expression on human health and use
this information to design specific interventions to treat
mitochondria-based disease and age-related pathology.
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Specifically, my lab
focuses on nucleus-encoded factors that are imported into the
organelle to regulate transcription, translation, replication, and
maintenance of mtDNA. We are also concerned with signaling pathways
that connect the nuclear and mitochondrial genomes to coordinate gene
expression patterns in both compartments. We use multiple approaches
to this problem including the employment of mouse and budding yeast
(S. cerevisiae) genetic model systems, biochemical
characterization of mitochondrial transcription events and
interactions, and in vivo approaches in cultured mammalian cells.
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| Contact Information: | | |
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