Extended Data Fig. 10: CXXC5 positively regulates BMP signaling.
(a) IGV tracks for RNA-seq and CXXC5 ChIP–seq (treated with vehicle or BMP4 for 2 hr) in TT150630 DIPG cells at BMP2, BMPR2 and ACVR1 gene loci. (b) Immunoblotting for phosphorylated SMAD1/5 (Ser 463/465), total SMAD1, CXXC5 and GAPDH in control and CXXC5 KD TT150714 DIPG cells. The experiments have been repeated three times with similar results. (c) Heatmaps of ChIP–seq signals of CXXC5 at top 4000 SMAD1 significant peaks or 5868 H3K27ac upregulated peaks respectively in TT150630 DIPG cells with or without BMP4 treatment for 2 hr (top). Average CXXC5 ChIP–seq signals corresponding with their ChIP–seq profiles in the indicated conditions (bottom). (d) Kaplan–Meier survival curves for DIPG patients in the UCSC xena patient cohort27, separated into ACVR1 high (n = 26 patients) and ACVR1 low (n = 25 patients) survival groups. Log-rank test was performed.
