ArticleNature genetics2017
Smarca4 ATPase mutations disrupt direct eviction of PRC1 from chromatin.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.
What it found
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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
130 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Nucleosome Turnover Regulates Histone Methylation Patterns over the Genome.Molecular cell · 2019Pooled it
- A bivalent molecular glue linking lysine acetyltransferases to oncogene-induced cell death.Cell · 2026Article
- Epigenetics in development, disease, and therapy: from mechanisms to clinical interventions.Science China. Life sciences · 2026Review
- Mutual antagonism between PRC1 condensates and SWI/SNF in chromatin regulation.Molecular cell · 2026Article
- Stem cell regulation: conserved pluripotency, transcriptional, and metabolic networks in animals and plants.Frontiers in cell and developmental biology · 2026Review
- Prognostic Implications of SMARCA4, ARID1A, and Other BAF Mutations in Non-Small Cell Lung Cancer.Cancer medicine · 2025Review
- Epigenetic reprogramming as the nexus of cancer stemness and therapy resistance: implications for biomarker discovery.Discover oncology · 2025Review
- Epigenetic control of cell identities from epiblast to gastrulation.The FEBS journal · 2025Review
- FET fusion oncoproteins enrich SWI/SNF complex subtypes and interaction partners.Cellular & molecular biology letters · 2025Article
- BRG1 Loss Is Frequent in Lung Cancer and Transforms Lung Epithelial Cells via Transcriptional and Epigenetic Reprograming.Cancers · 2025Article
- Mutual Antagonism Between PRC1 Condensates and SWI/SNF in Chromatin Regulation.bioRxiv : the preprint server for biology · 2025Article
- β-catenin functions as a molecular adapter for disordered cBAF interactions.Molecular cell · 2025Article
- Integrator promotes the association of TFIID and RNA polymerase II to maintain pluripotency during development.Molecular cell · 2025Article
- The role of SMARCA4 in lung cancer.Scientific reports · 2025Review
- SMARCA4 Inhibits Breast Cancer Progression and Metastasis through RHOA Suppression.Cancer research · 2025Article
- The SWI/SNF PBAF complex facilitates REST occupancy at repressive chromatin.Molecular cell · 2025Article
- PARP inhibition-associated heterochromatin confers increased DNA replication stress and vulnerability to ATR inhibition in SMARCA4-deficient cells.Cell death discovery · 2025Article
- Dysregulation of heterochromatin caused by genomic structural variants may be central to autism spectrum disorder.Frontiers in molecular neuroscience · 2025Article
- Differential modulation of polycomb-associated histone marks by cBAF, pBAF, and gBAF complexes.Life science alliance · 2024Article
- Preclinical evidence in the assembly of mammalian SWI/SNF complexes: Epigenetic insights and clinical perspectives in human lung disease therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Trithorax-group proteins and their mammalian homologs, including those in BAF (mSWI/SNF) complexes, are known to oppose the activity of Polycomb repressive complexes (PRCs). This opposition underlies the tumor-suppressive role of BAF subunits and is expected to contribute to neurodevelopmental disorders. However, the mechanisms underlying opposition to Polycomb silencing are poorly understood. Here we report that recurrent disease-associated mutations in BAF subunits induce genome-wide increases in PRC deposition and activity. We show that point mutations in SMARCA4 (also known as BRG1) mapping to the ATPase domain cause loss of direct binding between BAF and PRC1 that occurs independently of chromatin. Release of this direct interaction is ATP dependent, consistent with a transient eviction mechanism. Using a new chemical-induced proximity assay, we find that BAF directly evicts Polycomb factors within minutes of its occupancy, thereby establishing a new mechanism for the widespread BAF-PRC opposition underlying development and disease.
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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.