The premature ageing syndrome protein Cockayne Syndrome B modulates the repair of oxidative DNA lesions (2008)
- Autor:
- Autor USP: LARDNER, NADJA CRISTHINA DE SOUZA PINTO - IQ
- Unidade: IQ
- Subjects: BIOQUÍMICA; DANO AO DNA
- Language: Inglês
- Imprenta:
- Source:
- Título: Abstracts
- Conference titles: Reunião Anual da Sociedade Brasileira de Bioquímica e Biologia Molecular (SBBq)
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ABNT
SOUZA-PINTO, Nadja Cristhina de. The premature ageing syndrome protein Cockayne Syndrome B modulates the repair of oxidative DNA lesions. 2008, Anais.. São Paulo: SBBq, 2008. . Acesso em: 12 mar. 2026. -
APA
Souza-Pinto, N. C. de. (2008). The premature ageing syndrome protein Cockayne Syndrome B modulates the repair of oxidative DNA lesions. In Abstracts. São Paulo: SBBq. -
NLM
Souza-Pinto NC de. The premature ageing syndrome protein Cockayne Syndrome B modulates the repair of oxidative DNA lesions. Abstracts. 2008 ;[citado 2026 mar. 12 ] -
Vancouver
Souza-Pinto NC de. The premature ageing syndrome protein Cockayne Syndrome B modulates the repair of oxidative DNA lesions. Abstracts. 2008 ;[citado 2026 mar. 12 ] - Is mouse mitochondrial DNA protected from alkylation damage by AAG?
- Removal of oxidative DNA damage via FEN1-dependent long-patch base excision repair in human cell mitochondria
- Evidence that OGG1 glycosylase protects neurons against oxidative DNA damage and cell death under ischemic conditions
- PPAR coregulators are essential mediators of mitochondrial function and redox homeostasis in skeletal muscle cells
- ExoMeg1: a new exonuclease from metagenomic library
- Cockayne syndrome group B protein stimulates rapair of formamidopyrimidines by NEIL 1 DNA glycosylase
- The recombination protein RAD52 cooperates with the excision repair protein OGG1 for the repair of oxidative lesions in mammalian cells
- Molecular mechanisms for maintaining mitochondrial DNA stability in Alzheimer's disease
- Cell death induced by photoactive dyes depends on intracellular dye concentration and mitochondrial DNA damage
- Role of mTOR in the regulation of DNA repair activities in human mitochondria
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