Fiche publication
Date publication
juin 2024
Journal
Trends in cell biology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr EGLY Jean-Marc
Tous les auteurs :
Costanzo F, Paccosi E, Proietti-De-Santis L, Egly JM
Lien Pubmed
Résumé
To face genotoxic stress, eukaryotic cells evolved extremely refined mechanisms. Defects in counteracting the threat imposed by DNA damage underlie the rare disease Cockayne syndrome (CS), which arises from mutations in the CSA and CSB genes. Although initially defined as DNA repair proteins, recent work shows that CSA and CSB act instead as master regulators of the integrated response to genomic stress by coordinating DNA repair with transcription and cell division. CSA and CSB exert this function through the ubiquitination of target proteins, which are effectors/regulators of these processes. This review describes how the ubiquitination of target substrates is a common denominator by which CSA and CSB participate in different aspects of cellular life and how their mutation gives rise to the complex disease CS.
Mots clés
Cockayne syndrome (CS), DNA repair, genotoxic stress, transcription, ubiquitination
Référence
Trends Cell Biol. 2024 06 22;:
