Repair of Oxidative DNA Damage and Cancer: Recent Progress in DNA Base Excision Repair

Scott, Terrance M.; Rangaswamy, Suganya; Wicker, Christina A.; Izumi, Tohru

doi:10.1089/ars.2013.5529

Cited by 132 publications

(97 citation statements)

References 172 publications

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“…Furthermore, cell proliferation and apoptosis seem to be influenced by Ola1 (23). In both bacteria and humans, overexpression of YchF/Ola1 increases the sensitivity toward oxidative stress (53,56,57) and an imbalance of the oxidative stress response could potentially provide the link between DNA damage repair (40), the pathogenesis of multiple sclerosis (30), and apoptosis (43).…”

Section: Discussionmentioning

confidence: 99%

Redox Activation of the Universally Conserved ATPase YchF by Thioredoxin 1

Hannemann

Suppanz

et al. 2016

Antioxidants & Redox Signaling

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Aims: YchF/Ola1 are unconventional members of the universally conserved GTPase family because they preferentially hydrolyze ATP rather than GTP. These ATPases have been associated with various cellular processes and pathologies, including DNA repair, tumorigenesis, and apoptosis. In particular, a possible role in regulating the oxidative stress response has been suggested for both bacterial and human YchF/Ola1. In this study, we analyzed how YchF responds to oxidative stress and how it potentially regulates the antioxidant response. Results: Our data identify a redox-regulated monomer-dimer equilibrium of YchF as a key event in the functional cycle of YchF. Upon oxidative stress, the oxidation of a conserved and surface-exposed cysteine residue promotes YchF dimerization, which is accompanied by inhibition of the ATPase activity. No dimers were observed in a YchF mutant lacking this cysteine. In vitro, the YchF dimer is dissociated by thioredoxin 1 (TrxA) and this stimulates the ATPase activity. The physiological significance of the YchF-thioredoxin 1 interaction was demonstrated by in vivo cross-linking, which validated this interaction in living cells. This approach also revealed that both the ATPase domain and the helical domain of YchF are in contact with TrxA. Innovation: YchF/Ola1 are the first redox-regulated members of the universally conserved GTPase family and are inactivated by oxidation of a conserved cysteine residue within the nucleotide-binding motif. Conclusion: Our data provide novel insights into the regulation of the so far ill-defined YchF/Ola1 family of proteins and stipulate their role as negative regulators of the oxidative stress response. Antioxid. Redox Signal. 24, 141-156.

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Section: Discussionmentioning

confidence: 99%

Redox Activation of the Universally Conserved ATPase YchF by Thioredoxin 1

Hannemann

Suppanz

et al. 2016

Antioxidants & Redox Signaling

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“…Esse mecanismo é conhecido por reparo direto e ocorre de duas formas: reparo por excisão de base, conforme representado na Figura 2, ou reparo por excisão de nucleotídeos, esquematizado na Figura 3 (SCOTT et al, 2014). O reparo por excisão de base é desencadeado pela glicosilase, que promove a remoção da base alterada.…”

Section: Maquinário De Reparo Celularunclassified

“…Em seguida, a DNA polimerase preenche o espaço deixado, utilizando como molde a fita complementar não danificada. Para finalizar o processo, uma DNA ligase promove a ligação fosfodiéster entre o carbono três do nucleotídeo ao carbono cinco da pentose adjacente (SCOTT et al, 2014).…”

Section: Maquinário De Reparo Celularunclassified

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Mecanismos De Reparo Aos Danos No Dna Nos Pontos De Checagem Do Ciclo Celular

Nepomuceno¹,

Ferreira²,

Cruz³

et al. 2017

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RESUMOFrente aos avanços tecnológicos e no conhecimento, o entendimento dos mecanismos envolvidos na divisão celular e os diferentes fatores que controlam as fases do ciclo celular vêm ganhando destaque e uma nova compreensão a nível molecular. Ademais, compreender a interação complexa e diafonia entre os diferentes mecanismos de regulação com sobreposição e interação entre diferentes rotas, que competem ou colaboram para reparar um mesmo processo de injúria, conferem a reparação precisa dos danos exercidos ao DNA, processo de suma importância para a integridade do genoma. Em pretexto, esta revisão teve por objetivo descrever os mecanismos mais importantes que ocorrem em resposta aos danos do DNA de uma célula eucariótica, discutir a sua atividade através do ciclo celular e elucidar os principais mecanismos de regulação que influenciam na escolha das vias de reparação. PALAVRAS-CHAVE: Biologia Molecular; Divisão Celular; Neoplasia. REPAIR MECHANISMS TO DNA DAMAGES IN THE CELL CYCLE CHECKPOINTSABSTRACT Due to the advances in technology and in knowledge, the understanding of the mechanisms involved in cell division and the different factors that control the phases of cell cycle are gaining prominence and a new uptake in a molecular level. In addition, understand the crosstalk between the different mechanisms of regulation with overlapping and interaction between different routes, which compete or collaborate to repair the same injury process, is necessary to ensure the precise repair of damages in DNA, a process that is very important to the maintance of the integrity of the genome. In this way, this review aimed to describe the most important mechanisms that occur in response to damage in the DNA of a eukaryotic cell, to

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“…48 Hücre içi ROS artışı ve takiben ortaya çıkabi-lecek olası değişiklikler hem doğrudan DNA yapı-sını bozarak genotoksisiteye hem de epigenetik bir mekanizma ile DNA'nın etkilenmesine yol açar. [49][50][51] Çeşitli çalışmalar, ftalatlar dâhil olmak üzere PPAR-α agonistlerinin neden olduğu tümörogenez ile ROS arasında bir ilişki olduğunu göstermekte-dir. Bunun nedeni, bu kimyasal maddeler ile karaciğer parankimal hücrelerinde indüklenen farklı protein ve hücre organellerinin (peroksizom, mitokondri, mikrozom), özellikle H 2 O 2 ve diğer ok-sidanların neden olabileceği hasara açık olmaları-dır.…”

Section: R Re Ea Ak Kt Ti If F Ounclassified