Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.
Cell Mol Life Sci
; 73(16): 3097-114, 2016 08.
Article
em En
| MEDLINE
| ID: mdl-27094386
ABSTRACT
Interstrand crosslinks (ICLs) are a highly toxic form of DNA damage. ICLs can interfere with vital biological processes requiring separation of the two DNA strands, such as replication and transcription. If ICLs are left unrepaired, it can lead to mutations, chromosome breakage and mitotic catastrophe. The Fanconi anemia (FA) pathway can repair this type of DNA lesion, ensuring genomic stability. In this review, we will provide an overview of the cellular response to ICLs. First, we will discuss the origin of ICLs, comparing various endogenous and exogenous sources. Second, we will describe FA proteins as well as FA-related proteins involved in ICL repair, and the post-translational modifications that regulate these proteins. Finally, we will review the process of how ICLs are repaired by both replication-dependent and replication-independent mechanisms.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Dano ao DNA
/
DNA
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Transdução de Sinais
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Reagentes de Ligações Cruzadas
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Reparo do DNA
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Proteínas de Grupos de Complementação da Anemia de Fanconi
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Cell Mol Life Sci
Ano de publicação:
2016
Tipo de documento:
Article