Thomas Jefferson University - Michael P. King, Ph.D.
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Michael P. King, Ph.D.
Biochemistry and Molecular Biology
Thomas Jefferson University
Jefferson Medical College
Department of Biochemistry and Molecular Biology
Associate Professor
Ph.D., California Institute of Technology (1987)
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Mailing Address
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233 South 10th Street, 208 BLSB
Philadelphia, Pennsylvania 19107
United States
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Expertise and Research Interests
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Mitochondria are unusual among the organelles of a eukaryotic cell in that they possess their own genome, the mtDNA. The replication and transcription of mtDNA and the translation of the mtDNA-encoded proteins are essential for the production of ATP by oxidative phosphorylation. Mitochondrial diseases are a heterogeneous group of disorders that are defined by deficits of the mitochondrial respiratory chain. The research of this laboratory is directed towards investigations of mitochondrial biogenesis, the molecular genetic consequences of mtDNA mutations resulting in human disease, and potential genetic therapies for treatment of these diseases. Transmitochondrial cell models are used to investigate deficits of mitochondrial translation and respiratory chain activity that result from mtDNA mutations. Information derived from these studies is being applied to the development of genetic therapies for human diseases resulting from mutations in mtDNA.
Laboratory Staff
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Keywords
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Biochemistry; Molecular Genetics; Molecular Biology; Mitochondria; Human Disease; Neuromuscular Disease
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Publications
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- Sohm, B., Sissler, M. Park, H., King, M. P., and Florentz, C. (2004) Recognition of human mitochondrial tRNALeu(UUR) by its cognate leucyl-tRNA synthetase. Journal of Molecular Biology 339, 17-29.
- Mis, K., Mars, T., Jevsek, M., Strasek, H., Golicnik, M., Brecelj, J., Komel, R., King, M. P., Miranda, A. F., and Grubic, Z. (2005) Expression and distribution of acetylcholinesterase among the cellular components of the neuromuscular junction in human myotube in vitro. Chemico-Biological Interactions 157-158, 29-35.
- Kawamata, H., Magrane, J., Kunst, C., King, M. P., and Manfredi, G. (2008) Lysyl-tRNA synthetase is a target for mutant SOD1 toxicity in mitochondria. Journal of Biological Chemistry 283, 28321-28328.
- Park, H., Davidson, E., and King, M. P. (2008) Over-expressed mitochondrial leucyl-tRNA synthetase suppresses the A3243G mutation in the mitochondrial tRNALeu(UUR) gene. RNA 14, 2407-2416.
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Individual Expertise profile of
Michael P. King, Ph.D., Copyright © Michael P. King, Ph.D..
Last Updated
by Michael King, Ph.D. : Wednesday, March 18, 2009 10:12:05 AM
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