Fine-tuning the ubiquitin code at DNA double-strand breaks: deubiquitinating enzymes at work

Ubiquitination is a reversible protein modification broadly implicated in cellular functions. Signaling processes mediated by ubiquitin (ub) are crucial for the cellular response to DNA double-strand breaks (DSBs), one of the most dangerous types of DNA lesions. In particular, the DSB response criti...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Frontiers in genetics Jg. 6; S. 282
1. Verfasser: Citterio, Elisabetta
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers Media S.A 08.09.2015
Schlagworte:
Chromatin
Deubiquitinating enzymes
DNA damage response (DDR)
DNA Double-Strand Breaks (DSBs)
DUBs
Genetics
Ubiquitin
deubiquitinating enzymes (DUBs)
DNA damage response (DDR)
cancer
chromatin
hematopoietic stem cell (HSC)
histone H2A
ubiquitin
DNA double-strand breaks (DSBs)
ISSN:1664-8021, 1664-8021
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Ubiquitination is a reversible protein modification broadly implicated in cellular functions. Signaling processes mediated by ubiquitin (ub) are crucial for the cellular response to DNA double-strand breaks (DSBs), one of the most dangerous types of DNA lesions. In particular, the DSB response critically relies on active ubiquitination by the RNF8 and RNF168 ub ligases at the chromatin, which is essential for proper DSB signaling and repair. How this pathway is fine-tuned and what the functional consequences are of its deregulation for genome integrity and tissue homeostasis are subject of intense investigation. One important regulatory mechanism is by reversal of substrate ubiquitination through the activity of specific deubiquitinating enzymes (DUBs), as supported by the implication of a growing number of DUBs in DNA damage response processes. Here, we discuss the current knowledge of how ub-mediated signaling at DSBs is controlled by DUBs, with main focus on DUBs targeting histone H2A and on their recent implication in stem cell biology and cancer.
Bibliographie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
This article was submitted to Cancer Genetics, a section of the journal Frontiers in Genetics
Reviewed by: Richard Chahwan, Albert Einstein College of Medicine, USA; Anastasia Nijnik, McGill University, Canada
Edited by: Alessandra Montecucco, Consiglio Nazionale delle Ricerche, Italy
ISSN:1664-8021
1664-8021
DOI:10.3389/fgene.2015.00282