2dnk

Structural highlights

Function

CELF4_HUMAN RNA-binding protein implicated in the regulation of pre-mRNA alternative splicing. Mediates exon inclusion and/or exclusion in pre-mRNA that are subject to tissue-specific and developmentally regulated alternative splicing. Specifically activates exon 5 inclusion of cardiac isoforms of TNNT2 during heart remodeling at the juvenile to adult transition. Promotes exclusion of both the smooth muscle (SM) and non-muscle (NM) exons in actinin pre-mRNAs. Activates the splicing of MAPT/Tau exon 10. Binds to muscle-specific splicing enhancer (MSE) intronic sites flanking the alternative exon 5 of TNNT2 pre-mRNA.^{[1] [2] [3] [4] [5]}

Evolutionary Conservation

Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf.

References

1. ↑ Ladd AN, Charlet N, Cooper TA. The CELF family of RNA binding proteins is implicated in cell-specific and developmentally regulated alternative splicing. Mol Cell Biol. 2001 Feb;21(4):1285-96. PMID:11158314 doi:10.1128/MCB.21.4.1285-1296.2001
2. ↑ Gromak N, Matlin AJ, Cooper TA, Smith CW. Antagonistic regulation of alpha-actinin alternative splicing by CELF proteins and polypyrimidine tract binding protein. RNA. 2003 Apr;9(4):443-56. PMID:12649496
3. ↑ Wang J, Gao QS, Wang Y, Lafyatis R, Stamm S, Andreadis A. Tau exon 10, whose missplicing causes frontotemporal dementia, is regulated by an intricate interplay of cis elements and trans factors. J Neurochem. 2004 Mar;88(5):1078-90. PMID:15009664
4. ↑ Singh G, Charlet-B N, Han J, Cooper TA. ETR-3 and CELF4 protein domains required for RNA binding and splicing activity in vivo. Nucleic Acids Res. 2004 Feb 18;32(3):1232-41. Print 2004. PMID:14973222 doi:http://dx.doi.org/10.1093/nar/gkh275
5. ↑ Han J, Cooper TA. Identification of CELF splicing activation and repression domains in vivo. Nucleic Acids Res. 2005 May 13;33(9):2769-80. Print 2005. PMID:15894795 doi:http://dx.doi.org/10.1093/nar/gki561