Evidence map›Paper›PMID 36840360›Full record

ArticleAging cell2023

Transcriptional activation of Jun and Fos members of the AP-1 complex is a conserved signature of immune aging that contributes to inflammaging.

Emin Onur Karakaslar, Neerja Katiyar, Muneer Hasham, Ahrim Youn, Siddhartha Sharma, Cheng-Han Chung, Radu Marches, Ron Korstanje, Jacques Banchereau, Duygu Ucar

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
14.6field-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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Nuclear IDH3A Drives Transcriptional Programs in Melanoma via the YBX1-JUN/FOS Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  11. Transcription-based comparison ofMicrobiology spectrum · 2026
    Article
  12. Dysregulated Bone Marrow Contributes to Glomerular Injury through Soluble Factors.Journal of the American Society of Nephrology : JASN · 2026
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5 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

10 authors at 4 institutions in 2 countries.

Emin Onur KarakaslarThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.ORCID 0000-0002-9182-910X
Neerja KatiyarThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.ORCID 0000-0001-7414-9674
Muneer HashamThe Jackson Laboratory for Mammalian Genetics, Bar Harbor, Maine, USA.
Ahrim YounSanofi, Bridgewater, New Jersey, USA.
Siddhartha SharmaThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.
Cheng-Han ChungThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.ORCID 0000-0002-5412-1743
Radu MarchesThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.
Ron KorstanjeThe Jackson Laboratory for Mammalian Genetics, Bar Harbor, Maine, USA.
Jacques BanchereauThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.ORCID 0000-0003-3535-7221
Duygu UcarThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.ORCID 0000-0002-9772-3066
Jackson Laboratory · USImmunai (United States) · USLeiden University Medical Center · NLSanofi (United States) · US

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Paul Robson · 1985 to 2026
$61.9M
Translational CoreP30AG038070 · NIA · JACKSON LABORATORY · PI John Matthew Mahoney · 2010 to 2026
$19.3M
High-resolution single cell profiling of vaccine responsiveness in the elderlyR01AI142086 · NIAID · JACKSON LABORATORY · PI UCAR, DUYGU · 2019 to 2023
$2.9M
Genomics and Epigenomics of the Elderly Response to Pneumococcal VaccinesR01AG052608 · NIA · JACKSON LABORATORY · PI BANCHEREAU, JACQUES F · 2016 to 2019
$2.5M
Identification and Interpretation of Chromatin Changes Associated with the Aging of Human Immune CellsR35GM124922 · NIGMS · JACKSON LABORATORY · PI UCAR, DUYGU · 2017 to 2021
$2.3M
Physical Resiliencies: Indicators and Mechanisms in the Elderly CollaborativeUH2AG056925 · NIA · DUKE UNIVERSITY · PI COLON-EMERIC, CATHLEEN S, WHITSON, HEATHER E. · 2017 to 2018
$2.0M
NCI NIH HHS P30 CA034196NIAID NIH HHS R01 AI142086NIA NIH HHS P30 AG038070NIA NIH HHS R01 AG052608NIA NIH HHS UH2 AG056925NIGMS NIH HHS R35 GM124922NIH HHS R01 AG052608NIH HHS R01 AI142086NIH HHS UH2 AG056925
6 · The paper itself

Abstract

Diverse mouse strains have different health and life spans, mimicking the diversity among humans. To capture conserved aging signatures, we studied long-lived C57BL/6J and short-lived NZO/HILtJ mouse strains by profiling transcriptomes and epigenomes of immune cells from peripheral blood and the spleen from young and old mice. Transcriptional activation of the AP-1 transcription factor complex, particularly Fos, Junb, and Jun genes, was the most significant and conserved aging signature across tissues and strains. ATAC-seq data analyses showed that the chromatin around these genes was more accessible with age and there were significantly more binding sites for these TFs with age across all studied tissues, targeting pro-inflammatory molecules including Il6. Age-related increases in binding sites of JUN and FOS factors were also conserved in human peripheral blood ATAC-seq data. Single-cell RNA-seq data from the mouse aging cell atlas Tabula Muris Senis showed that the expression of these genes increased with age in B, T, NK cells, and macrophages, with macrophages from old mice expressing these molecules more abundantly than other cells. Functional data showed that upon myeloid cell activation via poly(I:C), the levels of JUN protein and its binding activity increased more significantly in spleen cells from old compared to young mice. In addition, upon activation, old cells produced more IL6 compared to young cells. In sum, we showed that the aging-related transcriptional activation of Jun and Fos family members in AP-1 complex is conserved across immune tissues and long- and short-living mouse strains, possibly contributing to increased inflammation with age.

Indexed as

Proto-Oncogene Proteins c-fosTranscription Factor AP-1AgingAnimalsHumansInterleukin-6MiceMice, Inbred C57BLProto-Oncogene Proteins c-junTranscriptional ActivationFos protein, mouseInterleukin-6Proto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junTranscription Factor AP-1agingepigenomehealthimmune aginginflammationlongevitymousetranscriptome

Identifiers

PMID36840360
PMCPMC10086525
OpenAlexW4321996737

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.