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	Provedor de dados Genet. Mol. Biol. (2) Autor Oliveira,Marcos T. (2) Ciesielski,Grzegorz L. (1) McKinney,Emily A. (1) Pontes,Carolina de Bovi (1) Palavra-chave DNA replication (2) Mitochondria (2) Pol γ (2) Twinkle (2) Human diseases (1) MtSSB (1) Mais... Tipo do documento Info:eu-repo/semantics/article (2) Ano 2020 (1) 2013 (1) País Brazil (2) Idioma Inglês (2)		Ordenar por:  Relevância Autor Título Ano Registros recuperados: 2 Primeira ... 1 ... Última Replicating animal mitochondrial DNA Genet. Mol. Biol. McKinney,Emily A.; Oliveira,Marcos T.. The field of mitochondrial DNA (mtDNA) replication has been experiencing incredible progress in recent years, and yet little is certain about the mechanism(s) used by animal cells to replicate this plasmid-like genome. The long-standing strand-displacement model of mammalian mtDNA replication (for which single-stranded DNA intermediates are a hallmark) has been intensively challenged by a new set of data, which suggests that replication proceeds via coupled leading-and lagging-strand synthesis (resembling bacterial genome replication) and/or via long stretches of RNA intermediates laid on the mtDNA lagging-strand (the so called RITOLS). The set of proteins required for mtDNA replication is small and includes the catalytic and accessory subunits of DNA... Tipo: Info:eu-repo/semantics/article Palavras-chave: DNA replication; Mitochondria; MtSSB; Pol γ; Twinkle. Ano: 2013 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572013000300002 Roles of the mitochondrial replisome in mitochondrial DNA deletion formation Genet. Mol. Biol. Oliveira,Marcos T.; Pontes,Carolina de Bovi; Ciesielski,Grzegorz L.. Abstract Mitochondrial DNA (mtDNA) deletions are a common cause of human mitochondrial diseases. Mutations in the genes encoding components of the mitochondrial replisome, such as DNA polymerase gamma (Pol γ) and the mtDNA helicase Twinkle, have been associated with the accumulation of such deletions and the development of pathological conditions in humans. Recently, we demonstrated that changes in the level of wild-type Twinkle promote mtDNA deletions, which implies that not only mutations in, but also dysregulation of the stoichiometry between the replisome components is potentially pathogenic. The mechanism(s) by which alterations to the replisome function generate mtDNA deletions is(are) currently under debate. It is commonly accepted that stalling of... Tipo: Info:eu-repo/semantics/article Palavras-chave: Mitochondria; DNA replication; Human diseases; Pol γ; Twinkle. Ano: 2020 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000200307 Registros recuperados: 2 Primeira ... 1 ... Última

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