Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination

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 bind...

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Autor principal:	Masamichi Ishiai
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	Fanconi anemia ubiquitination phosphorylation ATR ATM interstrand crosslink Genetics QH426-470
Acceso en línea:	https://doaj.org/article/48fb5e63ca36405db9f5bb01e9b0345c
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spelling	oai:doaj.org-article:48fb5e63ca36405db9f5bb01e9b0345c2021-11-25T17:41:39ZRegulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination10.3390/genes121117632073-4425https://doaj.org/article/48fb5e63ca36405db9f5bb01e9b0345c2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4425/12/11/1763https://doaj.org/toc/2073-4425The 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.Masamichi IshiaiMDPI AGarticleFanconi anemiaubiquitinationphosphorylationATRATMinterstrand crosslinkGeneticsQH426-470ENGenes, Vol 12, Iss 1763, p 1763 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Fanconi anemia ubiquitination phosphorylation ATR ATM interstrand crosslink Genetics QH426-470
spellingShingle	Fanconi anemia ubiquitination phosphorylation ATR ATM interstrand crosslink Genetics QH426-470 Masamichi Ishiai Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination
description	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.
format	article
author	Masamichi Ishiai
author_facet	Masamichi Ishiai
author_sort	Masamichi Ishiai
title	Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination
title_short	Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination
title_full	Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination
title_fullStr	Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination
title_full_unstemmed	Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination
title_sort	regulation of the fanconi anemia dna repair pathway by phosphorylation and monoubiquitination
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/48fb5e63ca36405db9f5bb01e9b0345c
work_keys_str_mv	AT masamichiishiai regulationofthefanconianemiadnarepairpathwaybyphosphorylationandmonoubiquitination
_version_	1718412101473533952

Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination

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