Evidence map›Paper›PMID 37922899›Full record

ArticleCell2023

Global identification of SWI/SNF targets reveals compensation by EP400.

Benjamin J E Martin, Eileen F Ablondi, Christine Goglia, Claudia A Mimoso, Piero R Espinel-Cabrera, Karen Adelman

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 74 citations in OpenAlex.

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  19. BAF complex-independent gene activation by SS18::SSX.bioRxiv : the preprint server for biology · 2026
    Article
  20. High-Efficiency Genomic Mapping of Chromatin-Associated Targets with CUT&RUN.Methods in molecular biology (Clifton, N.J.) · 2026
    Article

6 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Benjamin J E MartinDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA; Ludwig Center at Harvard, Boston, MA 02115, USA.
Eileen F AblondiDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Christine GogliaDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Claudia A MimosoDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Piero R Espinel-CabreraDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Karen AdelmanDepartment of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA; Ludwig Center at Harvard, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: karen_adelman@hms.harvard.edu.
Harvard University · USBroad Institute · US

Funding

Program in Genetics and Genomics PhD Training GrantT32GM141745 · NIGMS · HARVARD MEDICAL SCHOOL · PI Scott G Kennedy, Kamila Naxerova · 2021 to 2026
$3.6M
NIGMS NIH HHS T32 GM141745
6 · The paper itself

Abstract

Mammalian SWI/SNF chromatin remodeling complexes move and evict nucleosomes at gene promoters and enhancers to modulate DNA access. Although SWI/SNF subunits are commonly mutated in disease, therapeutic options are limited by our inability to predict SWI/SNF gene targets and conflicting studies on functional significance. Here, we leverage a fast-acting inhibitor of SWI/SNF remodeling to elucidate direct targets and effects of SWI/SNF. Blocking SWI/SNF activity causes a rapid and global loss of chromatin accessibility and transcription. Whereas repression persists at most enhancers, we uncover a compensatory role for the EP400/TIP60 remodeler, which reestablishes accessibility at most promoters during prolonged loss of SWI/SNF. Indeed, we observe synthetic lethality between EP400 and SWI/SNF in cancer cell lines and human cancer patient data. Our data define a set of molecular genomic features that accurately predict gene sensitivity to SWI/SNF inhibition in diverse cancer cell lines, thereby improving the therapeutic potential of SWI/SNF inhibitors.

Indexed as

Nuclear ProteinsTranscription FactorsAnimalsChromatinChromatin Assembly and DisassemblyDNA-Binding ProteinsDNA HelicasesHumansMiceNucleosomesChromatinDNA-Binding ProteinsDNA HelicasesEp400 protein, mouseNuclear ProteinsNucleosomesTranscription FactorsBRG1chromatin accessibilitychromatin remodelingcombination therapiesEP400epigenetic regulatorsPRO-seqRNAPIISWI/SNFtranscription

Identifiers

PMID37922899
PMCPMC11307202
OpenAlexW4388221419

What OpenQuestion holds

Textmetadata
LicenceTDM
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.