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Eiko Nakamaru-Ogiso, PhD
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Adjunct Professor of Pediatrics (Human Genetics)
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Research Laboratory Director, Mitochondrial Medicine Frontier Program, Children's Hospital of Philadelphia
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Department: Pediatrics
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Contact information
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Children’s Hospital of Philadelphia
30 Mitochondrial Medicine Frontier Program
2e Abramson Research Building (ARC) 1002A
39 3615 Civic Center Blvd
Philadelphia, PA 19104
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30 Mitochondrial Medicine Frontier Program
2e Abramson Research Building (ARC) 1002A
39 3615 Civic Center Blvd
Philadelphia, PA 19104
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Office: 215-590-6815
32 Fax: 215-590-0583
32 Lab: 215-590-6815
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32 Fax: 215-590-0583
32 Lab: 215-590-6815
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Email:
ogisoe@email.chop.edu
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ogisoe@email.chop.edu
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Publications
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Links
a5 Search PubMed for articles
a9 Research Laboratory Director, Mitochondrial Medicine Frontier Program
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a5 Search PubMed for articles
a9 Research Laboratory Director, Mitochondrial Medicine Frontier Program
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Education:
21 9 B.S. 25 (Biochemistry & Nutrition) c
2c University of Tokyo, 1988.
21 9 M.S. 25 (Biochemistry & Nutrition) c
2c University of Tokyo, 1990.
21 a Ph.D. 28 (Biochemistry & Neuroscience) c
2c University of Tokyo, 1998.
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Permanent link21 9 B.S. 25 (Biochemistry & Nutrition) c
2c University of Tokyo, 1988.
21 9 M.S. 25 (Biochemistry & Nutrition) c
2c University of Tokyo, 1990.
21 a Ph.D. 28 (Biochemistry & Neuroscience) c
2c University of Tokyo, 1998.
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257 The Ogiso's lab has been studying studying structure and function of bacterial/mitochondrial complex I, which is the entry enzyme of the respiratory chain. Complex I plays a central role in cellular aerobic energy metabolism. Therefore, complex I dysfunctions lead to a remarkably wide range of human diseases including heart failure, type 2 diabetes, and neuronal degenerative diseases such as Parkinson's Disease. Currently, we are tackling one of the most challenging fundamental questions in bioenergetics: How is electron transfer is linked to vectorial H+ translocation in complex I?
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249 We are also interested in how to rescue complex I dysfunction. The most crucial and unique function of complex I is NADH oxidation. Impaired NADH oxidation in mitochondria leads to lactic acidosis, high NADH/NAD+ ratio, increased reactive oxygen species (ROS), and eventually, apoptosis. One effective strategy is a complementation of dysfunctional complex I by fixing altered NADH/NAD+ balance to protect cells from excessive ROS generation. We are investigating the NAD+ metabolism in cells and animals, and searching for strategies to modulate NADH/NAD+ levels metabolically.
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Description of Research Expertise
32 Description of Research Expertise8
257 The Ogiso's lab has been studying studying structure and function of bacterial/mitochondrial complex I, which is the entry enzyme of the respiratory chain. Complex I plays a central role in cellular aerobic energy metabolism. Therefore, complex I dysfunctions lead to a remarkably wide range of human diseases including heart failure, type 2 diabetes, and neuronal degenerative diseases such as Parkinson's Disease. Currently, we are tackling one of the most challenging fundamental questions in bioenergetics: How is electron transfer is linked to vectorial H+ translocation in complex I?
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249 We are also interested in how to rescue complex I dysfunction. The most crucial and unique function of complex I is NADH oxidation. Impaired NADH oxidation in mitochondria leads to lactic acidosis, high NADH/NAD+ ratio, increased reactive oxygen species (ROS), and eventually, apoptosis. One effective strategy is a complementation of dysfunctional complex I by fixing altered NADH/NAD+ balance to protect cells from excessive ROS generation. We are investigating the NAD+ metabolism in cells and animals, and searching for strategies to modulate NADH/NAD+ levels metabolically.
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