DC Field | Value | Language |
---|---|---|
dc.contributor.author | Chen, Charlie Degui | ko |
dc.contributor.author | Kobayashi, Ryuji | ko |
dc.contributor.author | Helfman, David M | ko |
dc.date.accessioned | 2013-03-03T08:02:11Z | - |
dc.date.available | 2013-03-03T08:02:11Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 1999-03 | - |
dc.identifier.citation | GENES DEVELOPMENT, v.13, no.5, pp.593 - 606 | - |
dc.identifier.issn | 0890-9369 | - |
dc.identifier.uri | http://hdl.handle.net/10203/77885 | - |
dc.description.abstract | In the rat beta-tropomyosin (beta-TM) gene, exons 6 and 7 are spliced alternatively in a mutually exclusive manner. Exon 6 is included in mRNA encoding nonmuscle TM-1, whereas exon 7 is used in mRNA encoding skeletal muscle beta-TM. Previously, we demonstrated that a six nucleotide mutation at the 5' end of exon 7, designated as ex-1, activated exon 7 splicing in nonmuscle cells. In this study, we show that the activating effect of this mutation is not the result of creating an exonic splicing enhancer (ESE) or disrupting a putative secondary structure. The sequence in exon 7 acts as a bona fide exonic splicing silencer (ESS), which is bound specifically by a trans-acting factor. Isolation and peptide sequencing reveal that this factor is hnRNP H, a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family. Binding of hnRNP H correlates with the ESS activity. Furthermore, addition of antibodies that specifically recognizes hnRNP H to the splicing reactions or partial depletion of hnRNP H from nuclear extract activates exon 7 splicing in vitro and this effect can be reversed by addition of purified recombinant hnRNP E-I. These results indicate that hnRNP H participates in exclusion of exon 7 in nonmuscle cells. The involvement of hnRNP H in the activity of an ESS may represent a prototype for the regulation of tissue- and developmental-specific alternative splicing. | - |
dc.language | English | - |
dc.publisher | COLD SPRING HARBOR LAB PRESS | - |
dc.subject | PRE-MESSENGER-RNA | - |
dc.subject | IMMUNODEFICIENCY-VIRUS TYPE-1 | - |
dc.subject | SELECTION IN-VIVO | - |
dc.subject | PREMESSENGER RNA | - |
dc.subject | SR-PROTEINS | - |
dc.subject | SITE SELECTION | - |
dc.subject | 3&apos | - |
dc.subject | -SPLICE-SITE SELECTION | - |
dc.subject | SECONDARY STRUCTURE | - |
dc.subject | PRIMARY TRANSCRIPT | - |
dc.subject | CELLULAR FACTORS | - |
dc.title | Binding of hnRNP H to an exonic splicing silencer is involved in the regulation of alternative splicing of the rat beta-tropomyosin gene | - |
dc.type | Article | - |
dc.identifier.wosid | 000079163100010 | - |
dc.identifier.scopusid | 2-s2.0-0033105787 | - |
dc.type.rims | ART | - |
dc.citation.volume | 13 | - |
dc.citation.issue | 5 | - |
dc.citation.beginningpage | 593 | - |
dc.citation.endingpage | 606 | - |
dc.citation.publicationname | GENES DEVELOPMENT | - |
dc.identifier.doi | 10.1101/gad.13.5.593 | - |
dc.contributor.localauthor | Helfman, David M | - |
dc.contributor.nonIdAuthor | Chen, Charlie Degui | - |
dc.contributor.nonIdAuthor | Kobayashi, Ryuji | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | RNA processing | - |
dc.subject.keywordAuthor | cis-acting element | - |
dc.subject.keywordAuthor | trans-acting factor | - |
dc.subject.keywordAuthor | heterogeneous nuclear ribonucleoproteins | - |
dc.subject.keywordAuthor | RNA-protein interaction | - |
dc.subject.keywordPlus | PRE-MESSENGER-RNA | - |
dc.subject.keywordPlus | IMMUNODEFICIENCY-VIRUS TYPE-1 | - |
dc.subject.keywordPlus | SELECTION IN-VIVO | - |
dc.subject.keywordPlus | PREMESSENGER RNA | - |
dc.subject.keywordPlus | SR-PROTEINS | - |
dc.subject.keywordPlus | SITE SELECTION | - |
dc.subject.keywordPlus | 3&apos | - |
dc.subject.keywordPlus | -SPLICE-SITE SELECTION | - |
dc.subject.keywordPlus | SECONDARY STRUCTURE | - |
dc.subject.keywordPlus | PRIMARY TRANSCRIPT | - |
dc.subject.keywordPlus | CELLULAR FACTORS | - |
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