Fig. 4: AKAP8 antagonizes hnRNPM’s splicing activity. | Nature Communications

Fig. 4: AKAP8 antagonizes hnRNPM’s splicing activity.

From: The RNA-binding protein AKAP8 suppresses tumor metastasis by antagonizing EMT-associated alternative splicing

Fig. 4

a qRT-PCR (top) and semi-qPCR (bottom) analysis of CD44v8-splicing minigene assay showing that hnRNPM-mediated (hnM) exon skipping is antagonized by AKAP8 (AK8) in a dose-dependent manner. Incl: Inclusion. PSI: Percent Spliced In. b–c qRT-PCR (top) and semi-qPCR (bottom) analysis of CD44v5-splicing minigene assay showing that AKAP8 promotes v5 inclusion b and that AKAP8 inhibits hnRNPM-mediated exon skipping activity c. d, e Semi-qPCR of CD44v8 and CD44v5 minigene reporter assays showing increased exon skipping activity of hnRNPM in AKAP8 knockdown cells. f, g RNA pull-down assays showing that hnRNPM binds to its RNA cis-elements I-8 f and I-5 g more strongly in AKAP8-silenced epithelial HMLE cells. Twist-induced mesenchymal cells did not show binding differences. The sequences of I-8 and I-5 are shown at the bottom of each panel. Error bars indicate s.d. N = 3. (**) P < 0.01, (***) P < 0.001 between indicated groups. P values were tested by Student’s t test, two-tailed, in a, b, c. Source data are provided as a Source Data file.

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