Journal
GENES
Volume 12, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/genes12111763
Keywords
Fanconi anemia; ubiquitination; phosphorylation; ATR; ATM; interstrand crosslink; DNA repair
Categories
Funding
- JSPS KAKENHI [18K11642]
- Grants-in-Aid for Scientific Research [18K11642] Funding Source: KAKEN
Ask authors/readers for more resources
The Fanconi anemia (FA) DNA repair pathway is activated through monoubiquitination of FANCD2 and its binding partner FANCI, regulated by the ATR kinase. This process serves as a good example of ATR's contribution to genome stability.
The Fanconi anemia (FA) DNA repair pathway coordinates a faithful repair mechanism for stalled DNA replication forks caused by factors such as DNA interstrand crosslinks (ICLs) or replication stress. An important role of FA pathway activation is initiated by monoubiquitination of FANCD2 and its binding partner of FANCI, which is regulated by the ATM-related kinase, ATR. Therefore, regulation of the FA pathway is a good example of the contribution of ATR to genome stability. In this short review, we summarize the knowledge accumulated over the years regarding how the FA pathway is activated via phosphorylation and monoubiquitination.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available