IR@PKUHSC  > 北京大学基础医学院
学科主题基础医学
K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks
Zhu, B.1,2; Yan, K.1; Li, L.1; Lin, M.1; Zhang, S.1; He, Q.3; Zheng, D.4; Yang, H.1; Shao, G.1,2
刊名ONCOGENE
2015-05-28
DOI10.1038/onc.2014.229
34期:22页:2867-2878
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
研究领域[WOS]Biochemistry & Molecular Biology ; Oncology ; Cell Biology ; Genetics & Heredity
关键词[WOS]DOUBLE-STRAND BREAKS ; DAMAGE RESPONSE ; BINDING PROTEIN ; ANEMIA PATHWAY ; MONOUBIQUITINATED FANCD2 ; DEUBIQUITINATING ENZYME ; CANCER SUSCEPTIBILITY ; CHECKPOINT CONTROL ; MAMMALIAN-CELLS ; TARGETS BRCA1
英文摘要

DNA interstrand crosslinks (ICLs) are extremely deleterious lesions that are repaired by homologous recombination (HR) through coordination of Fanconi anemia (FA) proteins and breast cancer susceptibility gene 1 (BRCA1) product, but the exact role these proteins have remains unclear. Here we report that FANCG was modified by the addition of lysine63-linked polyubiquitin chains (K63Ub) in response to DNA damage. We show that FANCG K63Ub was dispensable for monoubiquitination of FANCD2, but was required for FANCG to interact with the Rap80-BRCA1 (receptor-associated protein 80-BRCA1) complex for subsequent modulation of HR repair of ICLs induced by mitomycin C. Mutation of three lysine residues within FANCG to arginine (K182, K258 and K347, 3KR) reduced FANCG K63Ub modification, as well as its interaction with the Rap80-BRCA1 complex, and therefore impeded HR repair. In addition, we demonstrated that K63Ub-modified FANCG was deubiquitinated by BRCC36 complex in vitro and in vivo. Inhibition of BRCC36 resulted in increased K63Ub modification of FANCG. Taken together, our results identify a new role of FANCG in HR repair of ICL through K63Ub-mediated interaction with the Rap80-BRCA1 complex.

语种英语
WOS记录号WOS:000355324300006
项目编号7122099 ; 81272915 ; 20110001110013 ; JWSL44-8
资助机构Beijing Natural Science Foundation ; Natural Science Foundation of China ; Research Fund for the Doctoral Program of Higher Education ; Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry ; 985 Program, Ministry of Education of China
引用统计
被引频次:9[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65860
专题北京大学基础医学院
作者单位1.Peking Univ, Sch Basic Med Sci, Dept fo Cell Biol, Beijing 100191, Peoples R China
2.Peking Univ, Inst Syst Biol, Beijing 100191, Peoples R China
3.Peking Univ, Ctr Med & Hlth Anal, Beijing 100191, Peoples R China
4.Shenzhen Univ, Sch Med, Shenzhen, Guangdong, Peoples R China
推荐引用方式
GB/T 7714
Zhu, B.,Yan, K.,Li, L.,et al. K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks[J]. ONCOGENE,2015,34(22):2867-2878.
APA Zhu, B..,Yan, K..,Li, L..,Lin, M..,Zhang, S..,...&Shao, G..(2015).K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks.ONCOGENE,34(22),2867-2878.
MLA Zhu, B.,et al."K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks".ONCOGENE 34.22(2015):2867-2878.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Zhu, B.]的文章
[Yan, K.]的文章
[Li, L.]的文章
百度学术
百度学术中相似的文章
[Zhu, B.]的文章
[Yan, K.]的文章
[Li, L.]的文章
必应学术
必应学术中相似的文章
[Zhu, B.]的文章
[Yan, K.]的文章
[Li, L.]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。