Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

H3-K27M-mutant nucleosomes interact with MLL1 to shape the glioma epigenetic landscape.

Cell reports - 17 May 2022

Furth Noa, Algranati Danielle, Dassa Bareket, Beresh Olga, Fedyuk Vadim, Morris Natasha, Kasper Lawryn H, Jones Dan, Monje Michelle, Baker Suzanne J, Shema Efrat

Abstract excerpt

Cancer-associated mutations in genes encoding histones dramatically reshape chromatin and support tumorigenesis. Lysine to methionine substitution of residue 27 on histone H3 (K27M) is a driver mutation in high-grade pediatric gliomas, known to abrogate polycomb repressive complex 2 (PRC2) activity. We applied single-molecule systems to image individual nucleosomes and delineate the combinatorial epigenetic...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Brain Neoplasms
Share to Chromatin

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Glioma

Share to Histone-Lysine N-Methyltransferase

Share to Histones

Share to Myeloid-Lymphoid Leukemia Protein

Share to Nucleosomes

Share to Polycomb Repressive Complex 2

Source

Identifiers

PMID: 35584667
DOI: 10.1016/j.celrep.2022.110836

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

H3-K27M-mutant nucleosomes interact with MLL1 to shape the glioma epigenetic landscape.PMID 35584667Read ↗

Oncohistone interactome profiling uncovers contrasting oncogenic mechanisms and identifies potential therapeutic targets in high grade glioma.Semantic proximity Read ↗

Histone H3 lysine-to-methionine mutants as a paradigm to study chromatin signaling.Semantic proximity Read ↗

Histone mutations in cancer.Semantic proximity Read ↗

H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programsSemantic proximity Read ↗

H3F3A K27M mutations drive a repressive transcriptome by modulating chromatin accessibility independent of H3K27me3 in Diffuse Midline Glioma.Semantic proximity Read ↗

Single-cell epigenetic analysis reveals principles of chromatin states in H3.3-K27M gliomas.Semantic proximity Read ↗

Evidence for coordinate CTCF and histone H3.3 activities in K27M diffuse midline gliomas.Semantic proximity Read ↗

Histone deposition pathways determine the chromatin landscapes of H3.1 and H3.3 K27M oncohistones.Semantic proximity Read ↗

Histone H3.3 K27M chromatin functions implicate a network of neurodevelopmental factors including ASCL1 and NEUROD1 in DIPG.Semantic proximity Read ↗

H2A.Z histone variants facilitate HDACi-dependent removal of H3.3K27M mutant protein in pediatric high-grade glioma cellsSemantic proximity Read ↗

H2A.Z histone variants facilitate HDACi-dependent removal of H3.3K27M mutant protein in paediatric high-grade glioma cellsSemantic proximity Read ↗

Multiomic screening platform uncovers the impact of histone mutations on chromatin and cell fateSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.