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学科主题: 基础医学
题名:
K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks
作者: 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
发表日期: 2015-05-28
DOI: 10.1038/onc.2014.229
卷: 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
所属项目编号: 7122099 ; 81272915 ; 20110001110013 ; JWSL44-8
项目资助者: 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
WOS记录号: WOS:000355324300006
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/65860
Appears in Collections:基础医学院_期刊论文

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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

Recommended Citation:
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.
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