The transcription factor FBI‐1 inhibits SAM68‐mediated BCL‐X alternative splicing and apoptosis. (10th February 2014)

• Record Type: Journal Article
• Authors: Bielli, Pamela; Busà, Roberta; Di Stasi, Savino M; Munoz, Manuel J; Botti, Flavia; Kornblihtt, Alberto R; Sette, Claudio
• Is Part Of: EMBO reports. Volume 15:Number 4(2014:Apr.)
• Page Start: 419
• Page End: 427
• Publication Date: 2014-02-10
• Subjects: Molecular biology -- Periodicals; Molecular Biology -- Periodicals; Molecular biology; Periodicals; 572.8
• DOI: 10.1002/embr.201338241
• Languages: English
• ISSNs: 1469-221X

Abstract

<abstract abstract-type="synopsis" xml:lang="en" id="embr201338241-abs-0002"> <title>Synopsis</title> <p> <boxed-text content-type="graphic" id="embr201338241-blkfxd-0001" position="anchor" orientation="portrait"> <graphic position="anchor" mimetype="image" xlink:href="ark:/27927/pghjsq57cj" orientation="portrait" xlink:type="simple" xmlns:xlink="http://www.w3.org/1999/xlink" /> </boxed-text> </p> <p>The oncogenic transcription factor FBI‐1 regulates alternative splicing by preventing the splicing regulator SAM68 from binding to BCL‐X mRNA. This increases anti‐apoptotic BCL‐X isoform expression and cell survival.</p> <p> <list id="embr201338241-list-0001" list-type="bullet"> <list-item> <p>The transcription factor FBI‐1 directly interacts with the splicing regulator SAM68.</p> </list-item> <list-item> <p>FBI‐1 impairs binding of SAM68 to BCL‐X mRNA and thus promotes production of the anti‐apoptotic BCL‐X isoform and cell survival.</p> </list-item> <list-item> <p>FBI‐1's effect on BCL‐X splicing requires histone deacetylase activity.</p> </list-item> </list> </p> </abstract>