CLC number:
On-line Access: 2023-12-08
Received: 2023-07-19
Revision Accepted: 2023-10-10
Crosschecked: 2023-12-12
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Yanhua MU, Jinhua HAN, Mingjie WU, Zongfang LI, Ke DU, Yameng WEI, Mengjie WU, Jun HUANG. Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites[J]. Journal of Zhejiang University Science B, 2023, 24(12): 1165-1173.
@article{title="Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites",
author="Yanhua MU, Jinhua HAN, Mingjie WU, Zongfang LI, Ke DU, Yameng WEI, Mengjie WU, Jun HUANG",
journal="Journal of Zhejiang University Science B",
volume="24",
number="12",
pages="1165-1173",
year="2023",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2300518"
}
%0 Journal Article
%T Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites
%A Yanhua MU
%A Jinhua HAN
%A Mingjie WU
%A Zongfang LI
%A Ke DU
%A Yameng WEI
%A Mengjie WU
%A Jun HUANG
%J Journal of Zhejiang University SCIENCE B
%V 24
%N 12
%P 1165-1173
%@ 1673-1581
%D 2023
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2300518
TY - JOUR
T1 - Fibrillarin promotes homologous recombination repair by facilitating the recruitment of recombinase RAD51 to DNA damage sites
A1 - Yanhua MU
A1 - Jinhua HAN
A1 - Mingjie WU
A1 - Zongfang LI
A1 - Ke DU
A1 - Yameng WEI
A1 - Mengjie WU
A1 - Jun HUANG
J0 - Journal of Zhejiang University Science B
VL - 24
IS - 12
SP - 1165
EP - 1173
%@ 1673-1581
Y1 - 2023
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2300518
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).
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