Evidence map›Paper›PMID 26842758›Full record

ArticleNature communications2016

Chromatin remodeller SMARCA4 recruits topoisomerase 1 and suppresses transcription-associated genomic instability.

Afzal Husain, Nasim A Begum, Takako Taniguchi, Hisaaki Taniguchi, Maki Kobayashi, Tasuku Honjo

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  6. The role of SMARCA4 in lung cancer.Scientific reports · 2025
    Review
  7. Article
  8. Article
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  14. Article
  15. Article
  16. Topoisomerases in Immune Cell Development and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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.

Afzal HusainDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe cho, Sakyo-ku, Kyoto 606-8501, Japan.
Nasim A BegumDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe cho, Sakyo-ku, Kyoto 606-8501, Japan.
Takako TaniguchiDivision of Disease Proteomics, Institute for Enzyme Research, University of Tokushima, Tokushima 770-8503, Japan.
Hisaaki TaniguchiDivision of Disease Proteomics, Institute for Enzyme Research, University of Tokushima, Tokushima 770-8503, Japan.
Maki KobayashiDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe cho, Sakyo-ku, Kyoto 606-8501, Japan.
Tasuku HonjoDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe cho, Sakyo-ku, Kyoto 606-8501, Japan.
Kyoto University · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Topoisomerase 1, an enzyme that relieves superhelical tension, is implicated in transcription-associated mutagenesis and genome instability-associated with neurodegenerative diseases as well as activation-induced cytidine deaminase. From proteomic analysis of TOP1-associated proteins, we identify SMARCA4, an ATP-dependent chromatin remodeller; FACT, a histone chaperone; and H3K4me3, a transcriptionally active chromatin marker. Here we show that SMARCA4 knockdown in a B-cell line decreases TOP1 recruitment to chromatin, and leads to increases in Igh/c-Myc chromosomal translocations, variable and switch region mutations and negative superhelicity, all of which are also observed in response to TOP1 knockdown. In contrast, FACT knockdown inhibits association of TOP1 with H3K4me3, and severely reduces DNA cleavage and Igh/c-Myc translocations, without significant effect on TOP1 recruitment to chromatin. We thus propose that SMARCA4 is involved in the TOP1 recruitment to general chromatin, whereas FACT is required for TOP1 binding to H3K4me3 at non-B DNA containing chromatin for the site-specific cleavage.

Indexed as

AnimalsB-LymphocytesCell Cycle ProteinsCell Line, TumorCell ProliferationChromatinChromatin Assembly and DisassemblyChromatin ImmunoprecipitationDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA CleavageDNA HelicasesDNA Topoisomerases, Type IFlow CytometryGene Knockdown TechniquesGenes, Immunoglobulin Heavy ChainCell Cycle ProteinsChromatinDNA-Binding ProteinsDNA HelicasesDNA Topoisomerases, Type IHigh Mobility Group ProteinsHistone ChaperonesNuclear ProteinsProteomeSMARCA4 protein, humanSmarca4 protein, mouseSSRP1 protein, humanSsrp1 protein, mouseSUPT16H protein, humanSupt16 protein, mouseTranscriptional Elongation FactorsTranscription Factors

Identifiers

PMID26842758
PMCPMC4742980
OpenAlexW2258552825

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.