Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites. / 纤维èç½éè¿ä¿è¿éç»é
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J Zhejiang Univ Sci B
; 24(12): 1165-1173, 2023 Dec 15.
Article
en En, Zh
| MEDLINE
| ID: mdl-38057273
ABSTRACT
Eukaryotic organisms constantly face a wide range of internal and external factors that cause damage to their DNA. Failure to accurately and efficiently repair these DNA lesions can result in genomic instability and the development of tumors (Canela et al., 2017). Among the various forms of DNA damage, DNA double-strand breaks (DSBs) are particularly harmful. Two major pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), are primarily responsible for repairing DSBs (Katsuki et al., 2020; Li and Yuan, 2021; Zhang and Gong, 2021; Xiang et al., 2023). NHEJ is an error-prone repair mechanism that simply joins the broken ends together (Blunt et al., 1995; Hartley et al., 1995). In contrast, HR is a precise repair process. It involves multiple proteins in eukaryotic cells, with the RAD51 recombinase being the key player, which is analogous to bacterial recombinase A (RecA) (Shinohara et al., 1992). The central event in HR is the formation of RAD51-single-stranded DNA (ssDNA) nucleoprotein filaments that facilitate homology search and DNA strand invasion, ultimately leading to the initiation of repair synthesis (Miné et al., 2007; Hilario et al., 2009; Ma et al., 2017).
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Proteínas de Unión al ADN
/
Reparación del ADN por Recombinación
Idioma:
En
/
Zh
Revista:
J Zhejiang Univ Sci B
Asunto de la revista:
BIOLOGIA
/
MEDICINA
Año:
2023
Tipo del documento:
Article
País de afiliación:
China