ArticleNature communications2024
PHF6 cooperates with SWI/SNF complexes to facilitate transcriptional progression.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- Comprehensive genomics and functional analyses identifyTranslational cancer research · 2026Article
- PHIP suppresses NuRD to enable the growth of SWI/SNF-mutant cancers.Nature communications · 2026Article
- Regulation of physical activity and energy expenditure through Phf6 in the medial preoptic area.Nature communications · 2026Article
- Regulation of stress susceptibility by chromatin-binding protein PHF6 in the pituitary intermediate lobe.Molecular psychiatry · 2026Article
- Phf6 truncating mutation drives leukemogenesis via disrupted epigenetic regulation in mice.Leukemia · 2026Article
- FBXO11 suppression rewires an NPM1-centered interactome influencing the progression of myelodysplastic syndrome.The Journal of clinical investigation · 2026Article
- Systematic Pan-Cancer Analysis Identifies PHF6 as an Immunological and Prognostic Biomarker.Diagnostics (Basel, Switzerland) · 2025Article
- A Coffin-Siris syndrome-associated mutation modeled in Caenorhabditis elegans affects multiple developmental processes.G3 (Bethesda, Md.) · 2025Article
- Leukemia mutated proteins PHF6 and PHIP form a chromatin complex that represses acute myeloid leukemia stemness.Genes & development · 2025Article
- CRISPR screen decodes SWI/SNF chromatin remodeling complex assembly.Nature communications · 2025Article
- Inflammatory metabolite 7α,25-OHC promotes TIMP1 expression in COVID-19 monocytes through synergy effect of SMARCC1/JUND/H3K27ac.Cellular and molecular life sciences : CMLS · 2025Article
- SMARCB1-deficient poorly differentiated testicular carcinoma: a case report.Frontiers in oncology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Genes encoding subunits of SWI/SNF (BAF) chromatin remodeling complexes are mutated in nearly 25% of cancers. To gain insight into the mechanisms by which SWI/SNF mutations drive cancer, we contributed ten rhabdoid tumor (RT) cell lines mutant for SWI/SNF subunit SMARCB1 to a genome-scale CRISPR-Cas9 depletion screen performed across 896 cell lines. We identify PHF6 as specifically essential for RT cell survival and demonstrate that dependency on Phf6 extends to Smarcb1-deficient cancers in vivo. As mutations in either SWI/SNF or PHF6 can cause the neurodevelopmental disorder Coffin-Siris syndrome, our findings of a dependency suggest a previously unrecognized functional link. We demonstrate that PHF6 co-localizes with SWI/SNF complexes at promoters, where it is essential for maintenance of an active chromatin state. We show that in the absence of SMARCB1, PHF6 loss disrupts the recruitment and stability of residual SWI/SNF complex members, collectively resulting in the loss of active chromatin at promoters and stalling of RNA Polymerase II progression. Our work establishes a mechanistic basis for the shared syndromic features of SWI/SNF and PHF6 mutations in CSS and the basis for selective dependency on PHF6 in SMARCB1-mutant cancers.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.