ArticleMolecular and cellular biology1997
Multiple interdependent sequence elements control splicing of a fibroblast growth factor receptor 2 alternative exon.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 85 citations in OpenAlex.
- Genetic Causes of Craniosynostosis: An Update.Molecular syndromology · 2019Review
- FGFR2 signaling underlies p63 oncogenic function in squamous cell carcinoma.The Journal of clinical investigation · 2013Article
- RBFOX2 is an important regulator of mesenchymal tissue-specific splicing in both normal and cancer tissues.Molecular and cellular biology · 2013Article
- Fox-3 and PSF interact to activate neural cell-specific alternative splicing.Nucleic acids research · 2011Article
- Article
- Role of RNA structure in regulating pre-mRNA splicing.Trends in biochemical sciences · 2010Review
- Autoregulation of Fox protein expression to produce dominant negative splicing factors.RNA (New York, N.Y.) · 2010Article
- Multiple splice defects in ABCA1 cause low HDL-C in a family with hypoalphalipoproteinemia and premature coronary disease.BMC medical genetics · 2009Article
- Combined use of MS2 and PP7 coat fusions shows that TIA-1 dominates hnRNP A1 for K-SAM exon splicing control.Journal of biomedicine & biotechnology · 2009Article
- Identification of an intronic splicing enhancer essential for the inclusion of FGFR2 exon IIIc.The Journal of biological chemistry · 2008Article
- Dunning rat prostate adenocarcinomas and alternative splicing reporters: powerful tools to study epithelial plasticity in prostate tumors in vivo.Clinical & experimental metastasis · 2008Article
- Imaging the alternative silencing of FGFR2 exon IIIb in vivo.RNA (New York, N.Y.) · 2006Article
- Alternative inclusion of fibroblast growth factor receptor 2 exon IIIc in Dunning prostate tumors reveals unexpected epithelial mesenchymal plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Fox-2 mediates epithelial cell-specific fibroblast growth factor receptor 2 exon choice.Molecular and cellular biology · 2006Article
- Homologues of the Caenorhabditis elegans Fox-1 protein are neuronal splicing regulators in mammals.Molecular and cellular biology · 2005Article
- A novel intronic cis element, ISE/ISS-3, regulates rat fibroblast growth factor receptor 2 splicing through activation of an upstream exon and repression of a downstream exon containing a noncanonical branch point sequence.Molecular and cellular biology · 2005Article
- Tissue-dependent isoforms of mammalian Fox-1 homologs are associated with tissue-specific splicing activities.Nucleic acids research · 2005Article
- Influence of RNA secondary structure on the pre-mRNA splicing process.Molecular and cellular biology · 2004Review
- An intronic enhancer regulates splicing of the twintron of Drosophila melanogaster prospero pre-mRNA by two different spliceosomes.Molecular and cellular biology · 2004Article
- RNA folding affects the recruitment of SR proteins by mouse and human polypurinic enhancer elements in the fibronectin EDA exon.Molecular and cellular biology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fibroblast growth factor receptor 2 gene contains a pair of mutually exclusive alternative exons, one of which (K-SAM) is spliced specifically in epithelial cells. We have described previously (F. Del Gatto and R. Breathnach, Mol. Cell. Biol. 15:4825-4834, 1995) some elements controlling K-SAM exon splicing, namely weak exon splice sites, an exon-repressing sequence, and an intron-activating sequence. We identify here two additional sequences in the intron downstream from the K-SAM exon which activate splicing of the exon. The first sequence (intron-activating sequence 2 [IAS2]) lies 168 to 186 nucleotides downstream from the exon's 5' splice site. The second sequence (intron-activating sequence 3 [IAS3]) lies 933 to 1,052 nucleotides downstream from the exon's 5' splice site. IAS3 is a complex region composed of several parts, one of which (nucleotides 963 to 983) can potentially form an RNA secondary structure with IAS2. This structure is composed of two stems separated by an asymmetric bulge. Mutations which disrupt either stem decrease activation, while compensatory mutations which reestablish the stem restore activation, either completely or partially, depending on the mutation. We present a model for K-SAM exon splicing involving the intervention of multiple, interdependent pre-mRNA sequence elements.
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