期刊
CELL REPORTS
卷 20, 期 2, 页码 297-307出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.06.056
关键词
-
类别
资金
- Japan Society for the Promotion of Science (JSPS) Research Fellowship for Young Scientists [13J02547]
- JSPS KAKENHI grants [JP16H04739, JP26650002, JP25116004, JP25131701, JP25125702, JP25116005, JP15K06942, JP15H01462]
- Matrix Science K. K., Mitsubishi, Asteras, Uehara
- Sumitomo
- Grants-in-Aid for Scientific Research [15K06942, 16H04739, 17H06426, 25116005, 13J02547] Funding Source: KAKEN
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据