RBM5/Luca-15/H37 Regulates Fas Alternative Splice Site Pairing after Exon Definition

被引：142

作者：

Bonnal, Sophie ^{[1
]}

Martinez, Concepcion ^{[1
]}

Foerch, Patrik ^{[4
]}

Bachi, Angela ^{[4
]}

Wilm, Matthias ^{[4
]}

Valcarcel, Juan ^{[1
,2
,3
]}

机构：

[1] Ctr Regulacio Genom, Barcelona 08003, Spain

[2] Inst Catalana Recerca & Estudis Avancats, Barcelona 08003, Spain

[3] Univ Pompeu Fabra, Barcelona 08003, Spain

[4] European Mol Biol Lab, D-69117 Heidelberg, Germany

来源：

MOLECULAR CELL | 2008年 / 32卷 / 01期

关键词：

D O I：

10.1016/j.molcel.2008.08.008

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：

RBM5/Luca-15/H37 is a gene frequently inactivated in lung cancers and overexpressed in breast tumors. Its protein product has been detected in prespliceosomal complexes and modulates cell proliferation and Fas-mediated apoptosis. We report that RBM5 is a component of complexes involved in 3' splice site recognition and regulates alternative splicing of apoptosis-related genes, including the Fas receptor, switching between isoforms with antagonistic functions in programmed cell death. In contrast with classical mechanisms of splicing regulation, RBM5 does not affect early events of splice site recognition that lead to Fas exon 6 definition. Instead, RBM5 inhibits the transition between prespliceosomal complexes assembled around exon 6 to mature spliceosomes assembled on the flanking introns and promotes sequence-specific pairing of the distal splice sites. An OCRE domain important for RBM5 function contacts components of the U4/5/6 tri-snRNP, consistent with the idea that RBM5 modulates splice site pairing after prespliceosome assembly and exon definition. a to

引用

页码：81 / 95

页数：15

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[1] The alternative genome [J].