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和文: 
英文:Inhibition of RIF1 by SCAI Allows BRCA1-Mediated Repair 
著者
和文: Isobe S. Y., Nagao K., Nozaki N., 木村 宏, Obuse C..  
英文: S. Y. Isobe, K. Nagao, N. Nozaki, H. Kimura, C. Obuse.  
言語 English 
掲載誌/書名
和文:Cell reports 
英文:Cell reports 
巻, 号, ページ Vol. 20    No. 2    pp. 297-307
出版年月 2017年7月11日 
出版者
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英文: 
会議名称
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英文: 
開催地
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英文: 
DOI https://doi.org/10.1016/j.celrep.2017.06.056
アブストラクト DNA double-strand breaks (DSBs) are repaired by either the homology-directed repair (HDR) or the non-homologous end-joining (NHEJ) pathway. RIF1 (RAP1-interacting factor homolog) was recently shown to stimulate NHEJ through an interaction with 53BP1 (p53-binding protein 1) phosphorylated at S/TQ sites, but the molecular mechanism underlying pathway choice remains unclear. Here, we show that SCAI (suppressor of cancer cell invasion) binds to 53BP1 phosphorylated at S/TP sites and facilitates HDR. Upon DNA damage, RIF1 immediately accumulates at damage sites and then gradually dissociates from 53BP1 and is subsequently replaced with SCAI. Depletion of SCAI reduces both the accumulation of HDR factors, including BRCA1 (breast cancer susceptibility gene 1), at damage sites and the efficiency of HDR, as detected by a reporter assay system. These data suggest that SCAI inhibits RIF1 function to allow BRCA1-mediated repair, which possibly includes alt-NHEJ and resection-dependent NHEJ in G1, as well as HDR in S/G2.

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