Restoration of mitochondrial function in cells with complex I deficiency

Yidong Bai; Jeong Soon Park; Jian Hong Deng; Youfen Li; Peiqing Hu

doi:10.1196/annals.1338.003

Restoration of mitochondrial function in cells with complex I deficiency

Yidong Bai, Jeong Soon Park, Jian Hong Deng, Youfen Li, Peiqing Hu

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

The mammalian mitochondrial NADH dehydrogenase (complex I) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To explore ways to restore mitochondrial function in complex I-deficient cells, various cell models with mutations in genes encoding subunits for complex I have been established. In this paper, we discuss various approaches to recover mitochondrial activity, the complex I activity in particular, in cultured cells.

Original language	English (US)
Pages (from-to)	25-35
Number of pages	11
Journal	Annals of the New York Academy of Sciences
Volume	1042
DOIs	https://doi.org/10.1196/annals.1338.003
State	Published - Jan 1 2005

Keywords

Complex I deficiency
NDI1
Restoration
Revertant
mtDNA mutation

ASJC Scopus subject areas

Neuroscience(all)
Biochemistry, Genetics and Molecular Biology(all)
History and Philosophy of Science

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title = "Restoration of mitochondrial function in cells with complex I deficiency",

abstract = "The mammalian mitochondrial NADH dehydrogenase (complex I) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To explore ways to restore mitochondrial function in complex I-deficient cells, various cell models with mutations in genes encoding subunits for complex I have been established. In this paper, we discuss various approaches to recover mitochondrial activity, the complex I activity in particular, in cultured cells.",

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AU - Bai, Yidong

AU - Park, Jeong Soon

AU - Deng, Jian Hong

AU - Li, Youfen

AU - Hu, Peiqing

PY - 2005/1/1

Y1 - 2005/1/1

N2 - The mammalian mitochondrial NADH dehydrogenase (complex I) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To explore ways to restore mitochondrial function in complex I-deficient cells, various cell models with mutations in genes encoding subunits for complex I have been established. In this paper, we discuss various approaches to recover mitochondrial activity, the complex I activity in particular, in cultured cells.

AB - The mammalian mitochondrial NADH dehydrogenase (complex I) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To explore ways to restore mitochondrial function in complex I-deficient cells, various cell models with mutations in genes encoding subunits for complex I have been established. In this paper, we discuss various approaches to recover mitochondrial activity, the complex I activity in particular, in cultured cells.

KW - Complex I deficiency

KW - NDI1

KW - Restoration

KW - Revertant

KW - mtDNA mutation

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Restoration of mitochondrial function in cells with complex I deficiency

Abstract

Keywords

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