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. 2013 Dec 15;126(24):5645–5656. doi: 10.1242/jcs.132985

Fig. 5.

Fig. 5.

IR isoform switching in post-confluent, differentiated Caco-2 cells and ApcMin/+ tumors is associated with altered expression of mRNAs encoding IR splicing enhancers and silencer. (A) Schematic summarizing prior in vitro work indicating RNA binding proteins that regulate IR isoform splicing from IR pre-mRNA. Splicing enhancers MBNL1, MBNL2 and SRSF3 promote exon 11 inclusion, favoring IR-B expression and silencer CUGBP1 promotes exon 11 exclusion, favoring IR-A (Sen et al., 2010; Sen et al., 2009). (B) qRT-PCR data showing levels of CUGBP1, MBNL2 and the ratio of MBNL2∶CUGBP1 expression in Caco-2 cells grown on Transwell plates for 2 days (undifferentiated/subconfluent) or 21 days post-confluence (differentiated). Data represent mean ± s.e.m. (n = 5); *P<0.05 versus subconfluent Caco-2 cells, paired t-test. (C, D) qRT-PCR measured Cugbp1, Mbnl2 and the ratios of Mbnl2∶Cugbp1 mRNA levels in small intestine (C) and/or colon (D) tumors from ApcMin/+ mice versus mucosal punch biopsies from normal small intestine and colon of wild-type (WT) mice. Data represent mean ± s.e.m. (n≧5); *P≤0.05 ApcMin/+ tumor versus WT tissue, unpaired t-test.