ArticleCell reports2018
The Tumor Suppressor ARID1A Controls Global Transcription via Pausing of RNA Polymerase II.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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
61 citing papers in PubMed, 102 citations in OpenAlex.
- Clonal lineage tracing and parallel multiomics profiling reveal transcriptional heterogeneity induced by ARID1A deficiency.Science advances · 2026Article
- A transient epithelial plasticity state defines the developmental window for uterine gland specification.bioRxiv : the preprint server for biology · 2026Article
- Arginine methylation of BAF155 regulates interactions with RNA processing machinery.bioRxiv : the preprint server for biology · 2026Article
- ADNP regulates chromatin architecture and lineage fidelity during neural differentiation.PLoS genetics · 2026Article
- Phosphoproteome landscape of ARID1A and its implications in DNA damage response and breast cancer pathogenesis.Discover oncology · 2026Article
- A Review of ARID1A's Role in Breast Cancer Progression: Context-Dependent Mechanisms and Therapeutic Implications.Cancers · 2025Review
- ARID1A stabilizes non-homologous end joining factors at DNA breaks induced by the G4 ligand pyridostatin.Cell reports · 2025Article
- YAP/TAZ: An epitome of tumorigenesis.Cancer letters · 2025Review
- Targeting USP8 causes synthetic lethality through degradation of FGFR2 in ARID1A-deficient ovarian clear cell carcinoma.NPJ precision oncology · 2025Article
- SWI/SNF Complex Connects Signaling and Epigenetic State in Cells of Nervous System.Molecular neurobiology · 2025Review
- Activity-assembled nBAF complex mediates rapid immediate early gene transcription by regulating RNA polymerase II productive elongation.Cell reports · 2024Article
- ARID1A-BAF coordinates ZIC2 genomic occupancy for epithelial-to-mesenchymal transition in cranial neural crest specification.American journal of human genetics · 2024Article
- Genome-Wide CRISPR Screen Identifies KEAP1 Perturbation as a Vulnerability of ARID1A-Deficient Cells.Cancers · 2024Article
- Protein destabilization underlies pathogenic missense mutations in ARID1B.Nature structural & molecular biology · 2024Article
- ARID1A loss activates MAPK signaling via DUSP4 downregulation.Journal of biomedical science · 2023Article
- Estrogen receptor alpha regulates uterine epithelial lineage specification and homeostasis.iScience · 2023Article
- G-quadruplexes associated with R-loops promote CTCF binding.Molecular cell · 2023Article
- Abnormal chromatin remodeling caused by ARID1A deletion leads to malformation of the dentate gyrus.Cell death and differentiation · 2023Article
- Oncogenic YAP mediates changes in chromatin accessibility and activity that drive cell cycle gene expression and cell migration.Nucleic acids research · 2023Article
- Transcriptional-translational conflict is a barrier to cellular transformation and cancer progression.Cancer cell · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
AT-rich interactive domain-containing proteins 1A and 1B (ARID1A and ARID1B) are mutually exclusive subunits of the chromatin remodeler SWI/SNF. ARID1A is the most frequently mutated chromatin regulator across all cancers, and ovarian clear cell carcinoma (OCCC) carries the highest prevalence of ARID1A mutations (∼57%). Despite evidence implicating ARID1A in tumorigenesis, the mechanism remains elusive. Here, we demonstrate that ARID1A binds active regulatory elements in OCCC. Depletion of ARID1A represses RNA polymerase II (RNAPII) transcription but results in modest changes to accessibility. Specifically, pausing of RNAPII is severely impaired after loss of ARID1A. Compromised pausing results in transcriptional dysregulation of active genes, which is compensated by upregulation of ARID1B. However, a subset of ARID1A-dependent genes is not rescued by ARID1B, including many p53 and estrogen receptor (ESR1) targets. Our results provide insight into ARID1A-mediated tumorigenesis and unveil functions of SWI/SNF in modulating RNAPII dynamics.
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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.