RBM10 regulates alternative splicing

被引:58
|
作者
Inoue, Akira [1 ,2 ]
Yamamoto, Naoki [3 ]
Kimura, Masatsugu [4 ]
Nishio, Koji [5 ]
Yamane, Hideo [2 ]
Nakajima, Koichi [1 ]
机构
[1] Osaka City Univ, Grad Sch Med, Dept Immunol, Osaka 5458585, Japan
[2] Osaka City Univ, Grad Sch Med, Dept Otolaryngol, Osaka 5458585, Japan
[3] Tokyo Med & Dent Univ, Grad Sch, Dept Psychiat & Behav Sci, Tokyo, Japan
[4] Osaka City Univ, Grad Sch Med, Dept Radioisotope Ctr, Osaka 5458585, Japan
[5] Nagoya Univ, Grad Sch Med, Dept Anat & Cell Biol, Nagoya, Aichi 4648601, Japan
关键词
S1-1; RBM10; RBM5; Alternative splicing; Fas; Bcl-x; SINGLE-STRANDED RNA; LUNG ADENOCARCINOMA; MOLECULAR-CLONING; TUMOR-SUPPRESSOR; FAS MOLECULE; ZINC FINGERS; CELL-DEATH; BCL-X; PROTEIN; GENE;
D O I
10.1016/j.febslet.2014.01.052
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
RBM10, originally called S1-1, is a nuclear RNA-binding protein with domains characteristic of RNA processing proteins. It has been reported that RBM10 constitutes spliceosome complexes and that RBM5, a close homologue of RBM10, regulates alternative splicing of apoptosis-related genes, Fas and cFLIP. In this study, we examined whether RBM10 has a regulatory function in splicing similar to RBM5, and determined that it indeed regulates alternative splicing of Fas and Bcl-x genes. RBM10 promotes exon skipping of Fas pre-mRNA as well as selection of an internal 5'-splice site in Bcl-x pre-mRNA. We propose a consensus RBM10-binding sequence at 5'-splice sites of target exons and a mechanistic model of RBM10 action in the alternative splicing. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:942 / 947
页数:6
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