ArticleNature communications2019
PFA ependymoma-associated protein EZHIP inhibits PRC2 activity through a H3 K27M-like mechanism.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
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Who cites it
140 citing papers in PubMed, 206 citations in OpenAlex.
- Targeted therapies plus radiotherapy for diffuse intrinsic pontine glioma: the randomized phase 2 BIOMEDE trial.Nature medicine · 2026Trial
- AOSNP-ADAPTR resource level-based recommendations on practical diagnostic strategies for ependymomas.Brain pathology (Zurich, Switzerland) · 2026Article
- Posterior fossa ependymoma: a comprehensive review of molecular classification, management guidelines, and clinical outcomes (Part I of ependymomas across compartments).Journal of neuro-oncology · 2026Review
- Review
- CXorf67 in malignancies: Deciphering epigenetic landscapes and clinical implications for precision oncology.Genes & diseases · 2026Review
- From chromatin dynamics to brain disease: Polycomb-Trithorax mechanisms in neurodevelopment.Trends in neurosciences · 2026Review
- Opposing function of AEBP2 isoforms fine-tune PRC2 catalytic activity.Nucleic acids research · 2026Article
- Feasibility of long-read nanopore sequencing for methylation-based classification of posterior fossa ependymomas.Brain tumor pathology · 2026Article
- Histone mark remodeling in cancer: an enhancer-centered perspective.Genes & genomics · 2026Review
- H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs.Nature genetics · 2026Article
- A brief history of ependymoma.Neuro-oncology · 2026Review
- Diffuse Midline Gliomas: Clinical, Diagnostic, and Therapeutic Perspectives.Biomedicines · 2026Review
- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- Article
- Polycomb repressive-deubiquitinase complex safeguards oocyte epigenome and female fertility by restraining Polycomb activity.Nature communications · 2026Article
- Emerging structural insights into PRC2 function in development and disease.Trends in biochemical sciences · 2026Review
- From Classical to Emerging Biomarkers of Brain and Central Nervous System Tumors. An Evidence-Based Review with a Focus on Gliomas.Cellular and molecular neurobiology · 2026Review
- EZHIP in Pediatric Brain Tumors: From Epigenetic Mimicry to Therapeutic Vulnerabilities.International journal of molecular sciences · 2026Review
- H3K27me3-dependent imprinting and transcriptional regulation in early mouse embryos requires EZHIP-mediated restriction of PRC2 activity.Nature communications · 2026Article
- EPOP restricts PRC2.1 targeting to chromatin by directly modulating enzyme complex dimerization.Nature communications · 2026Article
80 more citing papers are in PubMed but not listed here.
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14 authors at 6 institutions in 2 countries.
Funding
Abstract
Posterior fossa type A (PFA) ependymomas exhibit very low H3K27 methylation and express high levels of EZHIP (Enhancer of Zeste Homologs Inhibitory Protein, also termed CXORF67). Here we find that a conserved sequence in EZHIP is necessary and sufficient to inhibit PRC2 catalytic activity in vitro and in vivo. EZHIP directly contacts the active site of the EZH2 subunit in a mechanism similar to the H3 K27M oncohistone. Furthermore, expression of H3 K27M or EZHIP in cells promotes similar chromatin profiles: loss of broad H3K27me3 domains, but retention of H3K27me3 at CpG islands. We find that H3K27me3-mediated allosteric activation of PRC2 substantially increases the inhibition potential of EZHIP and H3 K27M, providing a mechanism to explain the observed loss of H3K27me3 spreading in tumors. Our data indicate that PFA ependymoma and DIPG are driven in part by the action of peptidyl PRC2 inhibitors, the K27M oncohistone and the EZHIP 'oncohistone-mimic', that dysregulate gene silencing to promote tumorigenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.