ArticleMolecular and cellular biology1998
An intronic sequence element mediates both activation and repression of rat fibroblast growth factor receptor 2 pre-mRNA splicing.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 104 citations in OpenAlex.
- The discovery, function, and regulation of epithelial splicing regulatory proteins (ESRP) 1 and 2.Biochemical Society transactions · 2023Article
- Alternative Pre-mRNA Splicing of the Mu Opioid Receptor Gene,Biomolecules · 2021Review
- A drug-repositioning screen using splicing-sensitive fluorescent reporters identifies novel modulators of VEGF-A splicing with anti-angiogenic properties.Oncogenesis · 2021Article
- Genetic Causes of Craniosynostosis: An Update.Molecular syndromology · 2019Review
- Angiogenesis-related pathways in the pathogenesis of ovarian cancer.International journal of molecular sciences · 2013Review
- Cleavage and polyadenylation specificity factor 1 (CPSF1) regulates alternative splicing of interleukin 7 receptor (IL7R) exon 6.RNA (New York, N.Y.) · 2013Article
- A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.Nature medicine · 2012Article
- Understanding the language of Lys36 methylation at histone H3.Nature reviews. Molecular cell biology · 2012Review
- A functional alternative splicing mutation in human tryptophan hydroxylase-2.Molecular psychiatry · 2011Article
- Epstein-Barr Virus SM protein utilizes cellular splicing factor SRp20 to mediate alternative splicing.Journal of virology · 2010Article
- Fox-2 protein regulates the alternative splicing of scleroderma-associated lysyl hydroxylase 2 messenger RNA.Arthritis and rheumatism · 2010Article
- hnRNP H and hnRNP F complex with Fox2 to silence fibroblast growth factor receptor 2 exon IIIc.Molecular and cellular biology · 2008Article
- Epstein-Barr virus SM protein functions as an alternative splicing factor.Journal of virology · 2008Article
- 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
- Fas-activated serine/threonine phosphoprotein (FAST) is a regulator of alternative splicing.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- The 3' untranslated region complex involved in stabilization of human alpha-globin mRNA assembles in the nucleus and serves an independent role as a splice enhancer.Molecular and cellular biology · 2007Article
- 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
- Identification of RNA-binding proteins that regulate FGFR2 splicing through the use of sensitive and specific dual color fluorescence minigene assays.RNA (New York, N.Y.) · 2006Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alternative splicing of fibroblast growth factor receptor 2 (FGF-R2) is an example of highly regulated alternative splicing in which exons IIIb and IIIc are utilized in a mutually exclusive manner in different cell types. The importance of this splicing choice is highlighted by studies which indicate that deregulation of the FGF-R2 splicing is associated with progression of prostate cancer. Loss of expression of a IIIb exon-containing isoform of FGF-R2 [FGF-R2 (IIIb)] accompanies the transition of a well-differentiated, androgen-dependent rat prostate cancer cell line, DT3, to the more aggressive, androgen-independent AT3 cell line. We have used transfection of rat FGF-R2 minigenes into DT3 and AT3 cancer cell lines to study the mechanisms that control alternative splicing of rat FGF-R2. Our results support a model in which an important cis-acting element located in the intron between these alternative exons mediates activation of splicing using the upstream IIIb exon and repression of the downstream IIIc exon in DT3 cells. This element consists of 57 nucleotides (nt) beginning 917 nt downstream of the IIIb exon. Analysis of mutants further demonstrates that an 18-nt "core sequence" within this element is most crucial for its function. Based on our observations, we have termed this sequence element ISAR (for intronic splicing activator and repressor), and we suggest that factors which bind this sequence are required for maintenance of expression of the FGF-R2 (IIIb) isoform.
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