Evidence map›Paper›PMID 39261837›Full record

ArticleCell communication and signaling : CCS2024

Bivalent chromatin accommodates survivin and BRG1/SWI complex to activate DNA damage response in CD4

Venkataragavan Chandrasekaran, Karin M E Andersson, Malin Erlandsson, Shuxiang Li, Torbjörn Nur Olsson, Maria-Jose Garcia-Bonete, Eric Malmhäll-Bah, Pegah Johansson, Gergely Katona, Maria I Bokarewa

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Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Insulin enables acquisition of the IL7RCell death & disease · 2026
    Article
  2. Review
  3. 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

10 authors.

Venkataragavan ChandrasekaranDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg, 40530, Sweden.
Karin M E AnderssonDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg, 40530, Sweden.
Malin ErlandssonDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg, 40530, Sweden.
Shuxiang LiComputational Biology and Biophysics Lab, Queen's University, Kingston, Canada.
Torbjörn Nur OlssonDepartment of Chemistry and Molecular Biology, Faculty of Science, University of Gothenburg, Gothenburg, Sweden.
Maria-Jose Garcia-BoneteDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, SE, 405 30, Sweden.
Eric Malmhäll-BahDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg, 40530, Sweden.
Pegah JohanssonDepartment of Clinical Chemistry, Sahlgrenska University Hospital, Gothenburg, Sweden.
Gergely KatonaDepartment of Chemistry and Molecular Biology, Faculty of Science, University of Gothenburg, Gothenburg, Sweden.
Maria I BokarewaDepartment of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Box 480, Gothenburg, 40530, Sweden. maria.bokarewa@rheuma.gu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBivalent regions of chromatin (BvCR) are characterized by trimethylated lysine 4 (H3K4me3) and lysine 27 on histone H3 (H3K27me3) deposition which aid gene expression control during cell differentiation. The role of BvCR in post-transcriptional DNA damage response remains unidentified. Oncoprotein survivin binds chromatin and mediates IFNγ effects in CD4

methodsWe performed deep sequencing of the chromatin bound to survivin, H3K4me3, H3K27me3, and H3K27ac, in human CD4

resultsWe identified that BvCR dominated by H3K4me3 (H3K4me3-BvCR) accommodated survivin within cis-regulatory elements of the genes controlling DNA damage. Inhibition of survivin or JAK-STAT signaling enhanced H3K4me3-BvCR dominance, which improved DNA damage recognition and arrested cell cycle progression in cultured CD4

conclusionsBvCR execute DNA damage control to maintain genome fidelity in IFN-activated CD4

Indexed as

CD4-Positive T-LymphocytesChromatinDNA DamageDNA HelicasesNuclear ProteinsSurvivinTranscription FactorsArthritis, RheumatoidHistonesHumansBIRC5 protein, humanChromatinDNA HelicasesHistonesNuclear ProteinsSMARCA4 protein, humanSurvivinTranscription FactorsAutoimmunityBivalent chromatinBRG1DNA damageSurvivin

Identifiers

PMID39261837
PMCPMC11389452

What Socratic holds

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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 Socratic graph.