Fig. 4: Oncohistone H3.3K27M primes CREB5 activation in DIPG. | Nature Communications

Fig. 4: Oncohistone H3.3K27M primes CREB5 activation in DIPG.

From: An oncohistone-driven H3.3K27M/CREB5/ID1 axis maintains the stemness and malignancy of diffuse intrinsic pontine glioma

Fig. 4

a Hi-C contact maps, RNA-seq, and ChIP-seq tracks of CTCF, H3K27me3, EZH2, H3K27ac, H3K4me1, H3K4me3, CpG islands (CGIs), and super-enhancer (SE) at HOXA1-13 and CREB5. The shading on the left denotes the promoter region of CREB5, while the shading on the right indicates the super-enhancer associated with CREB5. b qPCR analysis of CREB5 with or without H3.3K27M overexpression in PPC cells. c Immunoblotting analysis of the indicated proteins with or without H3.3K27M overexpression in PPC cells. d IGV tracks displaying H3K27M and H3K27me3 profiles in PPC cells at CREB5 locus and its neighboring HOXA1-13 gene cluster, with or without H3K27M OE. The blue shading denotes the differential binding peak of H3K27me3 at the promoter of CREB5. e qPCR analysis of H3.3K27M and CREB5 with or without H3.3K27M KD in DIPG17 cells. f Immunoblotting analysis of the indicated proteins with or without H3.3K27M KD in DIPG17 cells. g IGV tracks displaying H3K27me3 profile in DIPG17 cells at CREB5 and its neighboring HOXA1-13 gene cluster, with or without H3K27M KD. The blue shading denotes the differential binding peak of H3K27me3 at the promoter of CREB5. Data presented as mean ± s.e.m. of three independent experiments, statistical significance was determined by a two-tailed unpaired Student’s t-test (b and e). Experiments were repeated three times independently with similar results (c and f). Source data are provided as a Source Data file.

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