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Disruption of broad H3K9me3 domains and chromatin folding regulates oncogenic transcriptional milieu in ATRX-deficient gliomas [ChIP-seq]

ABSTRACT: To further understand the downstream epigenomic dysfunction induced by ATRX deficiency, we compared genome-wide chromatin-state maps of Atrx+ and Atrx- primary murine neuroepithelial progenitors (mNPCs). This ChIP–seq analysis revealed major differences in the localization of heterochromatin repressive marks H3K9me3 and H3K27me3. Specifically, we identified peculiar locations in the genome displaying H3K9me3 depletion and gain of H3K27me3 upon Atrx inactivation.

ORGANISM(S): Mus musculus

PROVIDER: GSE309141 | GEO | 2026/07/01

REPOSITORIES: GEO

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ATRX mutant neuroblastoma is sensitive to EZH2 inhibition via modulation of neuronal differentiation

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