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论文题目: RBM45 Competes with HDAC1 for Binding to FUS in Response to DNA Damage
论文题目英文:
作者: 巩娟娟①,#黄敏①,王凤丽①,#Xiao-Lu Ma,刘红美,涂英凤,#Ling-Yu Xing,朱雪霏,#Hui Zheng,#Jun-Jie Fang,李晓玲,王翘楚,王久强,#Zhong-Shuai Sun,王茜,汪蕴,#郭彩霞*,唐铁山*
论文出处:
年: 2017
卷:
期: DOI:10.1093/nar/gkx1102
页:
联系作者: #郭彩霞,唐铁山
发表期刊: Nucleic Acids Res
ISSN:
第一作者所在部门:
收录类别:
论文链接: https://academic.oup.com/nar/advance-article/doi/10.1093/nar/gkx1102/4621331
影响因子:
摘要: DNA damage response (DDR) is essential for genome stability and human health. Recently, several RNA binding proteins (RBPs), including fused-in-sarcoma (FUS), have been found unexpectedly to modulate this process. The role of FUS in DDR is closely linked to the pathogenesis of amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Given that RBM45 is also an ALS-associated RBP, we wondered whether RBM45 plays any function during this process. Here, we report that RBM45 can be recruited to laser microirradiation-induced DNA damage sites in a PAR- and FUS-dependent manner, but in a RNA-independent fashion. Depletion of RBM45 leads to abnormal DDR signaling and decreased efficiency in DNA double-stranded break repair. Interestingly, RBM45 is found to compete with histone deacetylase 1 (HDAC1) for binding to FUS, thereby regulating the recruitment of HDAC1 to DNA damage sites. A common familial ALS-associated FUS mutation (FUS-R521C) is revealed to prefer to cooperate with RBM45 than HDAC1. Our findings suggest that RBM45 is a key regulator in FUS-related DDR signaling whose dysfunction may contribute to the pathogenesis of ALS.
英文摘要:
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