Cargando…
Apn1 AP-endonuclease is essential for the repair of oxidatively damaged DNA bases in yeast frataxin-deficient cells
Frataxin deficiency results in mitochondrial dysfunction and oxidative stress and it is the cause of the hereditary neurodegenerative disease Friedreich ataxia (FA). Here, we present evidence that one of the pleiotropic effects of oxidative stress in frataxin-deficient yeast cells (Δyfh1 mutant) is...
Autores principales: | Lefevre, Sophie, Brossas, Caroline, Auchère, Françoise, Boggetto, Nicole, Camadro, Jean-Michel, Santos, Renata |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2012
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428155/ https://www.ncbi.nlm.nih.gov/pubmed/22706278 http://dx.doi.org/10.1093/hmg/dds230 |
Ejemplares similares
-
Apn1 and Apn2 endonucleases prevent accumulation of repair-associated DNA breaks in budding yeast as revealed by direct chromosomal analysis
por: Ma, Wenjian, et al.
Publicado: (2008) -
A Yeast/Drosophila Screen to Identify New Compounds Overcoming Frataxin Deficiency
por: Seguin, Alexandra, et al.
Publicado: (2015) -
Human mitochondrial ferritin improves respiratory function in yeast mutants deficient in iron–sulfur cluster biogenesis, but is not a functional homologue of yeast frataxin
por: Sutak, Robert, et al.
Publicado: (2012) -
AP endonuclease independent repair of abasic sites in Schizosaccharomyces pombe
por: Nilsen, Line, et al.
Publicado: (2012) -
AP endonuclease deficiency results in extreme sensitivity to thymidine deprivation
por: Dornfeld, Ken, et al.
Publicado: (2005)