ArticleNature genetics2017
SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters.
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 190 papers.
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
190 citing papers in PubMed, 287 citations in OpenAlex.
- Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026Review
- Delineating SWI/SNF gene and subtype expression in cancer.Epigenetics & chromatin · 2026Article
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- The CoREST complex inhibitor, corin, decreases tumor growth, increases cellular differentiation and extends lifespan in ATRT xenograft models.Neuro-oncology · 2026Article
- Epigenetic collapse establishes transcriptional bottlenecks in malignant rhabdoid tumor.Clinical epigenetics · 2026Review
- SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026Review
- Paediatric Therapeutic Development Workshop on rhabdoid tumours.British journal of cancer · 2026Review
- BCL7A's arginine anchor links nucleosome recognition to chromatin remodeling and diffuse large B-cell lymphoma tumor suppression.Protein & cell · 2026Article
- MeCP2 gene dosage-dependent neurodevelopmentally restricted defects arise by aberrant activation of cell fate-determining bivalent genes.Nature communications · 2026Article
- SMARCB1 missense mutants disrupt SWI/SNF complex stability and remodeling activity.Nature communications · 2026Article
- PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.Nature communications · 2026Article
- A SWI/SNF-specific Ig-like domain, SWIFT, is a transcription factor binding platform.Science (New York, N.Y.) · 2026Article
- Canonical BAF chromatin remodeling complex specifies stem cell fate via cell-type-specific co-factor recruitment.Nature communications · 2026Article
- Therapeutic targeting of chromatin alterations in leukemia and solid tumors.International journal of cancer · 2026Review
- Selective ARID1A Loss Restricted to the Undifferentiated Component of a Mismatch Repair-Deficient Gastric Carcinoma: A Case Report.Case reports in gastrointestinal medicine · 2026Article
- Decoding UTROSCT heterogeneity: systematic clinicopathological evaluation combined with molecular profiling.The journal of pathology. Clinical research · 2026Article
- Histogenesis of Atypical Teratoid Rhabdoid Tumors: Anatomical and Embryological Perspectives.Cancers · 2025Article
- Multi-omics profiling identified two epithelioid sarcoma molecular subtypes with distinct signaling and immune characteristics.Cancer communications (London, England) · 2025Article
- The SWI/SNF complex mediated chromatin remodeling promotes hepatitis B virus cccDNA transcription.Science China. Life sciences · 2025Article
- Targeting SUMOylation promotes cBAF complex stabilization and disruption of the SS18::SSX transcriptome in synovial sarcoma.Nature communications · 2025Article
130 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
Perturbations to mammalian SWI/SNF (mSWI/SNF or BAF) complexes contribute to more than 20% of human cancers, with driving roles first identified in malignant rhabdoid tumor, an aggressive pediatric cancer characterized by biallelic inactivation of the core BAF complex subunit SMARCB1 (BAF47). However, the mechanism by which this alteration contributes to tumorigenesis remains poorly understood. We find that BAF47 loss destabilizes BAF complexes on chromatin, absent significant changes in complex assembly or integrity. Rescue of BAF47 in BAF47-deficient sarcoma cell lines results in increased genome-wide BAF complex occupancy, facilitating widespread enhancer activation and opposition of Polycomb-mediated repression at bivalent promoters. We demonstrate differential regulation by two distinct mSWI/SNF assemblies, BAF and PBAF complexes, enhancers and promoters, respectively, suggesting that each complex has distinct functions that are perturbed upon BAF47 loss. Our results demonstrate collaborative mechanisms of mSWI/SNF-mediated gene activation, identifying functions that are co-opted or abated to drive human cancers and developmental disorders.
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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.