
Multiple layers of combinatorial interactions result in tissue-specific alternative splicing of FGFR2 transcripts. A schematic of exons 7–10 and introns 7–9 of FGFR2 is shown indicating that silencing of exon IIIb dominates in mesenchymal cells. In epithelial cells, however, a layer of regulation combines activation of exon 8 (IIIb) with repression of exon 9 (IIIc). These activities are mediated by two cis-elements: IAS2 and ISAR.










