Regulation of DNA cross-link repair by the Fanconi anemia/BRCA pathway

The maintenance of genome stability is critical for survival, and its failure is often associated with tumorigenesis. The Fanconi anemia (FA) pathway is essential for the repair of DNA interstrand cross-links (ICLs), and a germline defect in the pathway results in FA, a cancer predisposition syndrom...

Celý popis

Uloženo v:
Podrobná bibliografie
Vydáno v:Genes & development Ročník 26; číslo 13; s. 1393
Hlavní autoři: Kim, Hyungjin, D'Andrea, Alan D
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 01.07.2012
Témata:
Animals
DNA - metabolism
DNA Repair
Fanconi Anemia - genetics
Fanconi Anemia - metabolism
Fanconi Anemia Complementation Group Proteins - genetics
Fanconi Anemia Complementation Group Proteins - metabolism
Humans
Signal Transduction
ISSN:1549-5477, 1549-5477
On-line přístup:Zjistit podrobnosti o přístupu
Tagy: Přidat tag
Žádné tagy, Buďte první, kdo vytvoří štítek k tomuto záznamu!
Popis
Shrnutí:The maintenance of genome stability is critical for survival, and its failure is often associated with tumorigenesis. The Fanconi anemia (FA) pathway is essential for the repair of DNA interstrand cross-links (ICLs), and a germline defect in the pathway results in FA, a cancer predisposition syndrome driven by genome instability. Central to this pathway is the monoubiquitination of FANCD2, which coordinates multiple DNA repair activities required for the resolution of ICLs. Recent studies have demonstrated how the FA pathway coordinates three critical DNA repair processes, including nucleolytic incision, translesion DNA synthesis (TLS), and homologous recombination (HR). Here, we review recent advances in our understanding of the downstream ICL repair steps initiated by ubiquitin-mediated FA pathway activation.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1549-5477
1549-5477
DOI:10.1101/gad.195248.112