Evidence map›Paper›PMID 28481329›Full record

ArticleNature immunology2017

YAP antagonizes innate antiviral immunity and is targeted for lysosomal degradation through IKKɛ-mediated phosphorylation.

Shuai Wang, Feng Xie, Feng Chu, Zhengkui Zhang, Bing Yang, Tong Dai, Liang Gao, Lin Wang, Li Ling, Junling Jia and 4 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
9.3field-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

119 citing papers in PubMed, 196 citations in OpenAlex.

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59 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 3 countries.

Shuai WangJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Feng XieLife Sciences Institute and Innovation Center for Cell Signaling Network, Hangzhou, Zhejiang, China.
Feng ChuJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Zhengkui ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Hangzhou, Zhejiang, China.
Bing YangDepartment of Pharmaceutical Chemistry and the Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California, USA.
Tong DaiJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Liang GaoJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Lin WangJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Li LingJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Junling JiaLife Sciences Institute and Innovation Center for Cell Signaling Network, Hangzhou, Zhejiang, China.
Hans van DamDepartment of Molecular Cell Biology, Cancer Genomics Centre Netherlands, Leiden University Medical Center, Leiden, the Netherlands.
Jin JinLife Sciences Institute and Innovation Center for Cell Signaling Network, Hangzhou, Zhejiang, China.
Long ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Hangzhou, Zhejiang, China.
Fangfang ZhouJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu, China.
Soochow University · CNCancer Genomics Centre · NLUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription regulator YAP controls organ size by regulating cell growth, proliferation and apoptosis. However, whether YAP has a role in innate antiviral immunity is largely unknown. Here we found that YAP negatively regulated an antiviral immune response. YAP deficiency resulted in enhanced innate immunity, a diminished viral load, and morbidity in vivo. YAP blocked dimerization of the transcription factor IRF3 and impeded translocation of IRF3 to the nucleus after viral infection. Notably, virus-activated kinase IKKɛ phosphorylated YAP at Ser403 and thereby triggered degradation of YAP in lysosomes and, consequently, relief of YAP-mediated inhibition of the cellular antiviral response. These findings not only establish YAP as a modulator of the activation of IRF3 but also identify a previously unknown regulatory mechanism independent of the kinases Hippo and LATS via which YAP is controlled by the innate immune pathway.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsChemokine CCL5Chemokine CXCL10CRISPR-Cas SystemsFibroblastsFluorescent Antibody TechniqueGene EditingHEK293 CellsHeLa CellsHumansI-kappa B KinaseImmunity, InnateImmunoblottingImmunoprecipitationAdaptor Proteins, Signal TransducingCell Cycle ProteinsChemokine CCL5Chemokine CXCL10I-kappa B KinaseInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanIrf3 protein, mouseLATS1 protein, humanLATS2 protein, humanPhosphoproteinsProtein Serine-Threonine KinasesTumor Suppressor ProteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID28481329
OpenAlexW2613997270

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.