Evidence map›Paper›PMID 31015298›Full record

ArticleThe Journal of experimental medicine2019

Hes1 attenuates type I IFN responses via VEGF-C and WDFY1.

Fei Ning, Xiaoyu Li, Li Yu, Bin Zhang, Yuna Zhao, Yu Liu, Baohong Zhao, Yingli Shang, Xiaoyu Hu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  10. Secondary metabolites ofFrontiers in microbiology · 2023
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  13. Observational
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  15. Pen-2 Negatively Regulates the Differentiation of Oligodendrocyte Precursor Cells into Astrocytes in the Central Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. 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

9 authors at 5 institutions in 2 countries.

Fei NingInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Xiaoyu LiInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Li YuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.
Bin ZhangInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China.ORCID 0000-0001-6232-6768
Yuna ZhaoShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control & Prevention, College of Veterinary Medicine, Shandong Agricultural University, Taian, China.ORCID 0000-0002-4738-5193
Yu LiuState Key Laboratory of Virology, Medical Research Institute, College of Life Sciences, Wuhan University, Wuhan, China.
Baohong ZhaoArthritis and Tissue Degeneration Program, David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY.
Yingli ShangShandong Provincial Key Laboratory of Animal Biotechnology and Disease Control & Prevention, College of Veterinary Medicine, Shandong Agricultural University, Taian, China shangyl@sdau.edu.cn.ORCID 0000-0001-5052-8346
Xiaoyu HuInstitute for Immunology and School of Medicine, Tsinghua University, Beijing, China xiaoyuhu@tsinghua.edu.cn.ORCID 0000-0002-4289-6998
Tsinghua University · CNCenter for Life Sciences · CNShandong Agricultural University · CNHospital for Special Surgery · USWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of type I interferons (IFNs) is critical for eliciting competent immune responses, especially antiviral immunity. However, uncontrolled IFN production contributes to pathogenesis of autoimmune and inflammatory diseases. We found that transcription factor Hes1 suppressed production of type I IFNs and expression of IFN-stimulated genes. Functionally, Hes1-deficient mice displayed a heightened IFN signature in vivo, mounted enhanced resistance against encephalomyocarditis virus infection, and showed signs of exacerbated experimental lupus nephritis. Mechanistically, Hes1 did not suppress IFNs via direct transcriptional repression of IFN-encoding genes. Instead, Hes1 attenuated activation of TLR upstream signaling by inhibition of an adaptor molecule, WDFY1. Genome-wide assessment of Hes1 occupancy revealed that suppression of WDFY1 was secondary to direct binding and thus enhancement of expression of VEGF-C by Hes1, making

Indexed as

Adaptor Proteins, Signal TransducingAnimalsImmunityInterferon Type ILupus NephritisMacrophagesMice, Inbred C57BLSignal TransductionSwineToll-Like Receptor 3Transcription Factor HES-1Transcription, GeneticVascular Endothelial Growth Factor CAdaptor Proteins, Signal TransducingHes1 protein, mouseInterferon Type IToll-Like Receptor 3Transcription Factor HES-1Vascular Endothelial Growth Factor CWdfy1 protein, mouse

Identifiers

PMID31015298
PMCPMC6547865
OpenAlexW2941211633

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.