{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T02:29:30Z","timestamp":1790303370516,"version":"4.1.0"},"reference-count":71,"publisher":"The Company of Biologists","license":[{"start":{"date-parts":[[2021,5,18]],"date-time":"2021-05-18T00:00:00Z","timestamp":1621296000000},"content-version":"am","delay-in-days":2329,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>Alternative splicing (AS) is one of the major mechanisms to warrant the proteomic and functional diversity of eukaryotes. However, the complex nature of the splicing machinery, its associated splicing regulators and the functional implications of alternatively spliced transcripts is only poorly understood.<\/jats:p>\n               <jats:p>We investigated here the functional role of the splicing regulator rbfox1 in vivo using the zebrafish as a model system. We find that loss-of rbfox1 leads to progressive cardiac contractile dysfunction and heart failure. By using deep-transcriptome sequencing and quantitative real-time PCR we show that depletion of rbfox1 in zebrafish results in an altered isoform expression of several crucial target genes, such as actn3a and hug.<\/jats:p>\n               <jats:p>This study underlines that tightly regulated splicing is necessary for unconstrained cardiac function and renders the splicing regulator rbfox1 an interesting target to be investigated in human heart failure and cardiomyopathy.<\/jats:p>","DOI":"10.1242\/jcs.166850","type":"journal-article","created":{"date-parts":[[2015,6,27]],"date-time":"2015-06-27T11:53:09Z","timestamp":1435405989000},"source":"Crossref","is-referenced-by-count":13,"title":["RNA splicing regulated by RBFOX1 is essential for cardiac function in zebrafish"],"prefix":"10.1242","author":[{"given":"Karen S.","family":"Frese","sequence":"first","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin","family":"Meder","sequence":"additional","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"},{"name":"German Center for Cardiovascular Research, DZHK, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Keller","sequence":"additional","affiliation":[{"name":"Chair for Clinical Bioinformatics, Saarland University, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steffen","family":"Just","sequence":"additional","affiliation":[{"name":"Department of Medicine II, University of Ulm, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan","family":"Haas","sequence":"additional","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Britta","family":"Vogel","sequence":"additional","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon","family":"Fischer","sequence":"additional","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Backes","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Saarland University, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Matzas","sequence":"additional","affiliation":[{"name":"Department of Human Genetics, Saarland University, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Doreen","family":"K\u00f6hler","sequence":"additional","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vladimir","family":"Benes","sequence":"additional","affiliation":[{"name":"EMBL, European Molecular Biology Laboratory, Genomics Core Facility, Heidelberg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hugo A.","family":"Katus","sequence":"additional","affiliation":[{"name":"Department of Medicine III, University of Heidelberg, Heidelberg, Germany"},{"name":"German Center for Cardiovascular Research, DZHK, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wolfgang","family":"Rottbauer","sequence":"additional","affiliation":[{"name":"Department of Medicine II, University of Ulm, Ulm, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2015,1,1]]},"reference":[{"key":"2021042614381474100_JCS166850C1","doi-asserted-by":"publisher","first-page":"237","DOI":"10.1093\/hmg\/9.2.237","article-title":"Mutations affecting mRNA splicing are the most common molecular defects in patients with neurofibromatosis type 1","volume":"9","author":"Ars","year":"2000","journal-title":"Hum. 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