FIG. 7.

Model in which a combination of positive and negative effects leads to regulation of FGF-R2 alternative splicing. We propose that AT3 cells splice IIIc efficiently and skip exon IIIb as a result of the effect of ISS that is mediated in part by PTB. In DT3 cells, the same exon IIIb splicing silencing activity is present; however, it is counteracted by exon IIIb splicing activation, which includes factors that interact with ISAR. In addition, factors that interact with ISAR contribute to the repression of splicing of exon IIIc. Shaded boxes indicate ISS1 and ISS2 elements. Involvement of PTB with ISS1 is shown. Silencing effects, which involve ISS2 as well as less well characterized sequences downstream of exon IIIb are also proposed. The location and activity of ISAR and undefined protein(s) that bind to it are also shown.