Evidence map›Paper›PMID 34031145›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2021

NFAT5 Amplifies Antipathogen Responses by Enhancing Chromatin Accessibility, H3K27 Demethylation, and Transcription Factor Recruitment.

Giulia Lunazzi, Maria Buxadé, Marta Riera-Borrull, Laura Higuera, Sarah Bonnin, Hector Huerga Encabo, Silvia Gaggero, Diana Reyes-Garau, Carlos Company, Luca Cozzuto and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Life science alliance · 2024
    Article
  5. Article
  6. Inhibition of NFAT5-Dependent Astrocyte Swelling Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  7. N6-methyladenosine ofInternational journal of biological sciences · 2022
    Article
  8. Article
  9. Article
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

13 authors at 2 institutions in 1 country.

Giulia LunazziImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.ORCID 0000-0001-6859-9505
Maria BuxadéImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.ORCID 0000-0002-3020-8393
Marta Riera-BorrullImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.ORCID 0000-0003-4670-7290
Laura HigueraImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.ORCID 0000-0001-7723-492X
Sarah BonninCentre for Genomic Regulation, Barcelona, Spain.ORCID 0000-0001-5159-2518
Hector Huerga EncaboImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.
Silvia GaggeroImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.ORCID 0000-0002-2685-1108
Diana Reyes-GarauImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.
Carlos CompanyCentre for Genomic Regulation, Barcelona, Spain.
Luca CozzutoCentre for Genomic Regulation, Barcelona, Spain.ORCID 0000-0003-3194-8892
Julia PonomarenkoCentre for Genomic Regulation, Barcelona, Spain.
José AramburuImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain; cristina.lopez-rodriguez@upf.edu jose.aramburu@upf.edu.ORCID 0000-0001-9279-9523
Cristina López-RodríguezImmunology Unit, Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain; cristina.lopez-rodriguez@upf.edu jose.aramburu@upf.edu.ORCID 0000-0002-2311-2406
Universitat Pompeu Fabra · ESCentre for Genomic Regulation · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of innate immune cells to respond to pathogen-associated molecular patterns across a wide range of intensities is fundamental to limit the spreading of infections. Studies on transcription responses to pathogen-activated TLRs have often used relatively high TLR ligand concentrations, and less is known about their regulation under mild stimulatory conditions. We had shown that the transcription factor NFAT5 facilitates expression of antipathogen genes under TLR stimulation conditions corresponding to low pathogen loads. In this study, we analyze how NFAT5 optimizes TLR-activated responses in mouse macrophages. We show that NFAT5 was required for effective recruitment of central effectors p65/NF-κB and c-Fos to specific proinflammatory target genes, such as

Indexed as

AnimalsCells, CulturedChromatinDemethylationMiceMice, Inbred C57BLMice, KnockoutTranscription FactorsChromatinNfat5 protein, mouseTranscription Factors

Identifiers

PMID34031145
PMCPMC8176942
OpenAlexW3164293466

What OpenQuestion holds

Textmetadata
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.