Cargando…
Modulation of proteostasis counteracts oxidative stress and affects DNA base excision repair capacity in ATM-deficient cells
Ataxia telangiectasia (A-T) is a syndrome associated with loss of ATM protein function. Neurodegeneration and cancer predisposition, both hallmarks of A-T, are likely to emerge as a consequence of the persistent oxidative stress and DNA damage observed in this disease. Surprisingly however, despite...
Autores principales: | Poletto, Mattia, Yang, Di, Fletcher, Sally C., Vendrell, Iolanda, Fischer, Roman, Legrand, Arnaud J., Dianov, Grigory L. |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622344/ https://www.ncbi.nlm.nih.gov/pubmed/28973444 http://dx.doi.org/10.1093/nar/gkx635 |
Ejemplares similares
-
p53 coordinates base excision repair to prevent genomic instability
por: Poletto, Mattia, et al.
Publicado: (2016) -
Sp1 phosphorylation by ATM downregulates BER and promotes cell elimination in response to persistent DNA damage
por: Fletcher, Sally C, et al.
Publicado: (2018) -
Cells deficient in base-excision repair reveal cancer hallmarks originating from adjustments to genetic instability
por: Markkanen, Enni, et al.
Publicado: (2015) -
Phosphorylation of PNKP by ATM prevents its proteasomal degradation and enhances resistance to oxidative stress
por: Parsons, Jason L., et al.
Publicado: (2012) -
USP7S-dependent inactivation of Mule regulates DNA damage signalling and repair
por: Khoronenkova, Svetlana V., et al.
Publicado: (2013)