Evidence map›Paper›PMID 34731603›Full record

ArticleCell reports2021

Acute depletion of the ARID1A subunit of SWI/SNF complexes reveals distinct pathways for activation and repression of transcription.

Seraina Blümli, Nicola Wiechens, Meng-Ying Wu, Vijender Singh, Marek Gierlinski, Gabriele Schweikert, Nick Gilbert, Catherine Naughton, Ramasubramanian Sundaramoorthy, Joby Varghese and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 54 citations in OpenAlex.

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  5. BAF complex-independent gene activation by SS18::SSX.bioRxiv : the preprint server for biology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Seraina BlümliCentre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Nicola WiechensCentre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Meng-Ying WuCentre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Vijender SinghComputational Core, University of Connecticut, 67 North Eagleville Road, Storrs, CT 06269, USA.
Marek GierlinskiComputational Biology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Gabriele SchweikertComputational Biology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Nick GilbertMRC Human Genetics Unit, Institute of Genetics & Cancer, The University of Edinburgh, Edinburgh EH4 2XU, UK.
Catherine NaughtonMRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee DD1 5EH, UK.
Ramasubramanian SundaramoorthyCentre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK.
Joby VargheseMRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee DD1 5EH, UK.
Robert GourlayMRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee DD1 5EH, UK.
Renata SoaresMRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee DD1 5EH, UK.
David ClarkDivision of Developmental Biology, National Institute of Child Health and Human Development, NIH, Building 6A, 6 Centre Drive, Bethesda, MD 20892, USA.
Tom Owen-HughesCentre for Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. Electronic address: t.a.owenhughes@dundee.ac.uk.
University of Dundee · GBEunice Kennedy Shriver National Institute of Child Health and Human Development · USInstitute of Genetics and Cancer · GBUniversity of Connecticut · US

Funding

Cancer Research UK C1195/A17994Medical Research Council MR/S021647/1Medical Research Council MR/SO21647/1Medical Research Council MR/T022620/1
6 · The paper itself

Abstract

The ARID1A subunit of SWI/SNF chromatin remodeling complexes is a potent tumor suppressor. Here, a degron is applied to detect rapid loss of chromatin accessibility at thousands of loci where ARID1A acts to generate accessible minidomains of nucleosomes. Loss of ARID1A also results in the redistribution of the coactivator EP300. Co-incident EP300 dissociation and lost chromatin accessibility at enhancer elements are highly enriched adjacent to rapidly downregulated genes. In contrast, sites of gained EP300 occupancy are linked to genes that are transcriptionally upregulated. These chromatin changes are associated with a small number of genes that are differentially expressed in the first hours following loss of ARID1A. Indirect or adaptive changes dominate the transcriptome following growth for days after loss of ARID1A and result in strong engagement with cancer pathways. The identification of this hierarchy suggests sites for intervention in ARID1A-driven diseases.

Indexed as

Transcriptional ActivationTranscription, GeneticAnimalsBinding SitesCell LineChromatin Assembly and DisassemblyDNA-Binding ProteinsE1A-Associated p300 ProteinMaleMiceMice, 129 StrainMouse Embryonic Stem CellsNucleosomesPrecancerous ConditionsProteolysisTime FactorsArid1a protein, mouseDNA-Binding ProteinsE1A-Associated p300 ProteinEp300 protein, mouseNucleosomesTranscription FactorsARID1ABAFcancerchromatin remodelingenhancer transcriptionEP300nucleosomesSWI/SNF

Identifiers

PMID34731603
PMCPMC8578704
OpenAlexW3208197345

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.