hnRNP A1 and hnRNP F Modulate the Alternative Splicing of Exon 11 of the Insulin Receptor Gene
Figure 7
Model for antagonistic regulation of exon 11 inclusion by hnRNP A1 and hnRNP F/SRSF1.
When hnRNP A1 is highly expressed compared to SRSF1, binding of hnRNP A1 to the 5′ splice site of intron 11 and the intronic elements blocks recognition of the exon by the splicing apparatus causing skipping of the exon. When hnRNP A1 is low compared to SRSF1, binding of SRSF1 to the exon prevents binding of hnRNP A1 allowing binding of SRSF3 and hnRNP F that promote exon inclusion.