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FEBS Lett. 2014 Mar 18;588(6):942-7. doi: 10.1016/j.febslet.2014.01.052. Epub 2014 Feb 11.

RBM10 regulates alternative splicing.

Author information

1
Department of Immunology, Osaka City University Graduate School of Medicine, Japan; Department of Otolaryngology, Osaka City University Graduate School of Medicine, Japan. Electronic address: ainoue@med.osaka-cu.ac.jp.
2
Department of Psychiatry and Behavioral Sciences, Tokyo Medical and Dental University Graduate School, Japan.
3
Department of Radioisotope Center, Osaka City University Graduate School of Medicine, Japan.
4
Department of Anatomy and Cell Biology, Graduate School of Medicine, Nagoya University, Japan.
5
Department of Otolaryngology, Osaka City University Graduate School of Medicine, Japan.
6
Department of Immunology, Osaka City University Graduate School of Medicine, Japan.

Abstract

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.

KEYWORDS:

Alternative splicing; Bcl-x; Fas; RBM10; RBM5; S1-1

PMID:
24530524
DOI:
10.1016/j.febslet.2014.01.052
[Indexed for MEDLINE]
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