ArticleMolecular cell2025
The SWI/SNF PBAF complex facilitates REST occupancy at repressive chromatin.
Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed.
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- PBRM1-dependent PBAF targeting is required for EMT and metastasis in breast cancer.Science advances · 2026Article
- Cooperation of Transcription Factor PAX6 with Chromatin-Remodeling Complex BAF During Embryonic Development in Mammals.Cellular and molecular neurobiology · 2026Review
- β-catenin functions as a molecular adapter for disordered cBAF interactions.Molecular cell · 2025Article
- SMARCB1-related schwannomatosis and other SMARCB1-associated phenotypes: clinical spectrum and molecular pathogenesis.Familial cancer · 2025Review
- Subunits Med12 and Med13 of Mediator Cooperate with Subunits SAYP and Bap170 of SWI/SNF in Active Transcription inInternational journal of molecular sciences · 2024Article
Corrections and comments
- Update of
Authors and funding
13 authors.
Funding
Abstract
SWI/SNF (switch/sucrose non-fermentable) chromatin remodelers possess unique functionalities difficult to dissect. Distinct cancers harbor mutations in specific subunits, such as the polybromo-associated BAF (PBAF)-specific component ARID2 in melanoma. Here, we perform epigenomic profiling of SWI/SNF complexes and their associated chromatin states in melanocytes and melanoma. Time-resolved approaches reveal that PBAF regions are generally less sensitive to ATPase inhibition than BAF sites. We further uncover a subset of PBAF-exclusive regions within Polycomb-repressed chromatin that are enriched for REST (RE1 silencing transcription factor), a transcription factor that represses neuronal genes. In turn, PBAF complex disruption via ARID2 loss hinders REST's ability to bind and inactivate its targets, leading to upregulation of synaptic transcripts. Remarkably, this gene signature is conserved in melanoma patients with ARID2 mutations and correlates with an expression program enriched in melanoma brain metastases. Overall, we demonstrate a unique role for PBAF in generating accessibility for a silencing transcription factor at repressed chromatin, with important implications for disease.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.