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- W2112163917 endingPage "10887" @default.
- W2112163917 startingPage "10870" @default.
- W2112163917 abstract "In normal cells, mitochondria are the primary organelles that generate energy, which is critical for cellular metabolism. Mitochondrial dysfunction, caused by mitochondrial DNA (mtDNA) mutations or an abnormal mtDNA copy number, is linked to a range of human diseases, including Alzheimer's disease, premature aging and cancer. mtDNA resides in the mitochondrial lumen, and its duplication requires the mtDNA replicative helicase, Twinkle. In addition to Twinkle, many DNA helicases, which are encoded by the nuclear genome and are crucial for nuclear genome integrity, are transported into the mitochondrion to also function in mtDNA replication and repair. To date, these helicases include RecQ-like helicase 4 (RECQ4), petite integration frequency 1 (PIF1), DNA replication helicase/nuclease 2 (DNA2) and suppressor of var1 3-like protein 1 (SUV3). Although the nuclear functions of some of these DNA helicases have been extensively studied, the regulation of their mitochondrial transport and the mechanisms by which they contribute to mtDNA synthesis and maintenance remain largely unknown. In this review, we attempt to summarize recent research progress on the role of mammalian DNA helicases in mitochondrial genome maintenance and the effects on mitochondria-associated diseases." @default.
- W2112163917 created "2016-06-24" @default.
- W2112163917 creator A5074801223 @default.
- W2112163917 creator A5082109293 @default.
- W2112163917 date "2015-05-13" @default.
- W2112163917 modified "2023-09-27" @default.
- W2112163917 title "Borrowing Nuclear DNA Helicases to Protect Mitochondrial DNA" @default.
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