ArticleeLife2020
Histone deposition pathways determine the chromatin landscapes of H3.1 and H3.3 K27M oncohistones.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- ONC201/dordaviprone for H3 K27M-mutant tumors: Discovery, mechanisms, therapeutic potential, and future directions.Genes & diseases · 2027Review
- Article
- Histone H3K27M variants determine myeloid subset dependencies and immune reprogramming in diffuse midline glioma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Novel modifiers of oncoprotein-mediated Polycomb inhibition in Drosophila melanogaster.Genetics · 2025Article
- A histone methyltransferase-independent function of PRC2 controls small RNA dynamics during programmed DNA elimination in Paramecium.Nucleic acids research · 2025Article
- Implications of canonical histone H3.1 and histone variant H3.3 in cancer.Open biology · 2025Review
- Investigating oncoprotein-mediated chromatin dysregulation inbioRxiv : the preprint server for biology · 2025Article
- The length of the G1 phase is an essential determinant of H3K27me3 landscapes across diverse cell types.PLoS biology · 2025Article
- Elucidating neuroepigenetic mechanisms to inform targeted therapeutics for brain disorders.iScience · 2025Review
- The histone H3.3 K27M mutation suppresses Ser31phosphorylation and mitotic fidelity, which can directly drive gliomagenesis.Current biology : CB · 2025Article
- Multi-omics approaches reveal that diffuse midline gliomas present altered DNA replication and are susceptible to replication stress therapy.Genome biology · 2024Article
- An E2 ubiquitin-conjugating enzyme links diubiquitinated H2B to H3K27M oncohistone function.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Histone H3 mutations and their impact on genome stability maintenance.Biochemical Society transactions · 2024Review
- The H3.3K36M oncohistone disrupts the establishment of epigenetic memory through loss of DNA methylation.Molecular cell · 2024Article
- Roles of Histone H2B, H3 and H4 Variants in Cancer Development and Prognosis.International journal of molecular sciences · 2024Review
- H3K27M mutant glioma: Disease definition and biological underpinnings.Neuro-oncology · 2024Review
- Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors.Nucleic acids research · 2024Article
- Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies.Genome biology · 2023Article
- The cell-cycle choreography of H3 variants shapes the genome.Molecular cell · 2023Review
- Leveraging dominant-negative histone H3 K-to-M mutations to study chromatin during differentiation and development.Development (Cambridge, England) · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Lysine 27-to-methionine (K27M) mutations in the H3.1 or H3.3 histone genes are characteristic of pediatric diffuse midline gliomas (DMGs). These oncohistone mutations dominantly inhibit histone H3K27 trimethylation and silencing, but it is unknown how oncohistone type affects gliomagenesis. We show that the genomic distributions of H3.1 and H3.3 oncohistones in human patient-derived DMG cells are consistent with the DNAreplication-coupled deposition of histone H3.1 and the predominant replication-independent deposition of histone H3.3. Although H3K27 trimethylation is reduced for both oncohistone types, H3.3K27M-bearing cells retain some domains, and only H3.1K27M-bearing cells lack H3K27 trimethylation. Neither oncohistone interferes with PRC2 binding. Using
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Registered trials
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.