| http://purl.uniprot.org/citations/11158314 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11158314 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11158314 | http://www.w3.org/2000/01/rdf-schema#comment | "Alternative splicing of cardiac troponin T (cTNT) exon 5 undergoes a developmentally regulated switch such that exon inclusion predominates in embryonic, but not adult, striated muscle. We previously described four muscle-specific splicing enhancers (MSEs) within introns flanking exon 5 in chicken cTNT that are both necessary and sufficient for exon inclusion in embryonic muscle. We also demonstrated that CUG-binding protein (CUG-BP) binds a conserved CUG motif within a human cTNT MSE and positively regulates MSE-dependent exon inclusion. Here we report that CUG-BP is one of a novel family of developmentally regulated RNA binding proteins that includes embryonically lethal abnormal vision-type RNA binding protein 3 (ETR-3). This family, which we call CELF proteins for CUG-BP- and ETR-3-like factors, specifically bound MSE-containing RNAs in vitro and activated MSE-dependent exon inclusion of cTNT minigenes in vivo. The expression of two CELF proteins is highly restricted to brain. CUG-BP, ETR-3, and CELF4 are more broadly expressed, and expression is developmentally regulated in striated muscle and brain. Changes in the level of expression and isoforms of ETR-3 in two different developmental systems correlated with regulated changes in cTNT splicing. A switch from cTNT exon skipping to inclusion tightly correlated with induction of ETR-3 protein expression during differentiation of C2C12 myoblasts. During heart development, the switch in cTNT splicing correlated with a transition in ETR-3 protein isoforms. We propose that ETR-3 is a major regulator of cTNT alternative splicing and that the CELF family plays an important regulatory role in cell-specific alternative splicing during normal development and disease."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.21.4.1285-1296.2001"xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.21.4.1285-1296.2001"xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/author | "Cooper T.A."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/author | "Cooper T.A."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/author | "Ladd A.N."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/author | "Ladd A.N."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/author | "Charlet-B N."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/author | "Charlet-B N."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/date | "2001"xsd:gYear |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/name | "Mol. Cell. Biol."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/name | "Mol. Cell. Biol."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/pages | "1285-1296"xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/pages | "1285-1296"xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/title | "The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/title | "The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing."xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/volume | "21"xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://purl.uniprot.org/core/volume | "21"xsd:string |
| http://purl.uniprot.org/citations/11158314 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11158314 |
| http://purl.uniprot.org/citations/11158314 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/11158314 |
| http://purl.uniprot.org/citations/11158314 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11158314 |
| http://purl.uniprot.org/citations/11158314 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/11158314 |