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- W2103010054 abstract "The intronic splicing silencer (ISS) of CFTR exon 9 promotes exclusion of this exon from the mature mRNA. This negative influence has important consequences with regards to human pathologic events, as lack of exon 9 correlates well with the occurrence of monosymptomatic and full forms of CF disease. We have previously shown that the ISS element interacts with members of the SR protein family. In this work, we now provide the identification of SF2/ASF and SRp40 as the specific SR proteins binding to this element and map their precise binding sites in IVS9. We have also performed a functional analysis of the ISS element using a variety of unrelated SR-binding sequences and different splicing systems. Our results suggest that SR proteins mediate CFTR exon 9 exclusion by providing a 'decoy' sequence in the vicinity of its suboptimal donor site. The results of this study give an insight on intron 'exonization' mechanisms and provide useful indications for the development of novel therapeutic strategies aimed at the recovery of exon inclusion." @default.
- W2103010054 created "2016-06-24" @default.
- W2103010054 creator A5029821144 @default.
- W2103010054 creator A5031651201 @default.
- W2103010054 creator A5032436476 @default.
- W2103010054 creator A5083854775 @default.
- W2103010054 date "2007-06-18" @default.
- W2103010054 modified "2023-10-01" @default.
- W2103010054 title "SR protein-mediated inhibition of CFTR exon 9 inclusion: molecular characterization of the intronic splicing silencer" @default.
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- W2103010054 doi "https://doi.org/10.1093/nar/gkm444" @default.
- W2103010054 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1935002" @default.
- W2103010054 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17576688" @default.
- W2103010054 hasPublicationYear "2007" @default.
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