Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers.
Nat Rev Mol Cell Biol
; 17(6): 379-94, 2016 05 23.
Article
en En
| MEDLINE
| ID: mdl-27211488
ABSTRACT
DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions. The swift recognition and faithful repair of such damage is crucial for the maintenance of genomic stability, as well as for cell and organismal fitness. Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs) orchestrates and regulates cellular responses to DSBs at multiple levels, often involving extensive crosstalk between these modifications. Recent findings have revealed compelling insights into the complex mechanisms by which ubiquitin and UBLs regulate protein interactions with DSB sites to promote accurate lesion repair and protection of genome integrity in mammalian cells. These advances offer new therapeutic opportunities for diseases linked to genetic instability.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Ubiquitina
/
Reparación del ADN
/
Roturas del ADN de Doble Cadena
/
Ubiquitinación
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Nat Rev Mol Cell Biol
Asunto de la revista:
BIOLOGIA MOLECULAR
Año:
2016
Tipo del documento:
Article
País de afiliación:
Dinamarca