Evidence map›Paper›PMID 28346439›Full record

ArticleNature cell biology2017

Hippo signalling governs cytosolic nucleic acid sensing through YAP/TAZ-mediated TBK1 blockade.

Qian Zhang, Fansen Meng, Shasha Chen, Steven W Plouffe, Shiying Wu, Shengduo Liu, Xinran Li, Ruyuan Zhou, Junxian Wang, Bin Zhao and 6 more

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
8.9field-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

133 citing papers in PubMed, 201 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 2 countries.

Qian ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Fansen MengLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Shasha ChenLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Steven W PlouffeDepartment of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, California 92093, USA.
Shiying WuLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Shengduo LiuLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Xinran LiLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Ruyuan ZhouLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Junxian WangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Bin ZhaoLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Jianming LiuDepartment of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Jun QinThe Key Laboratory of Stem Cell Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Jian ZouEye Center of the Second Affiliated Hospital School of Medicine, Institutes of Translational Medicine, Zhejiang University, Hangzhou 310058, China.
Xin-Hua FengLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.
Kun-Liang GuanDepartment of Pharmacology and Moores Cancer Center, University of California San Diego, La Jolla, California 92093, USA.
Pinglong XuLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou 310058, China.ORCID 0000-0001-7726-5443
Zhejiang University · CNUniversity of California San Diego · USBaylor College of Medicine · USBoston Children's Hospital · USChinese Academy of Sciences · CNSecond Affiliated Hospital of Zhejiang University · CN

Funding

GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
PROTEIN PHOSPHORYLATION AND GROWTH FACTOR FUNCTIONR01GM051586 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROWN, JOAN HELLER · 1994 to 2024
$7.9M
The mTOR and Hippo pathway in cell growth and cancerR35CA196878 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUAN, KUN-LIANG · 2015 to 2019
$4.0M
TSC2 tumor suppressor protein in cell energy responseR01CA108941 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GUAN, KUN-LIANG · 2004 to 2015
$3.8M
Regulation and function of the YAP transcription co-activator oncoproteinR01CA132809 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUAN, KUN-LIANG · 2008 to 2015
$2.6M
Regulation of the Hippo pathway and its role in uveal melanomaR01EY022611 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUAN, KUN-LIANG · 2012 to 2015
$1.5M
ALK causes TGF-beta insensitivity in lung cancer cellsR21CA209007 · NCI · BAYLOR COLLEGE OF MEDICINE · PI FENG, XIN-HUA · 2016 to 2017
$379k
NCI NIH HHS R01 CA108941NCI NIH HHS R01 CA132809NCI NIH HHS R21 CA209007NCI NIH HHS R35 CA196878NEI NIH HHS R01 EY022611NHLBI NIH HHS T32 HL007572NIGMS NIH HHS R01 GM051586NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defence. The correlation between cellular nutrient/physical status and host antiviral defence is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through the transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 Lys63-linked ubiquitylation and the binding of adaptors/substrates. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defence in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defence.

Indexed as

Signal TransductionAcyltransferasesAdaptor Proteins, Signal TransducingAnimalsAntiviral AgentsCytosolDNADoxorubicinFluorescent Antibody TechniqueGene Expression RegulationHEK293 CellsHippo Signaling PathwayHumansInterferon Regulatory Factor-3LysineMice, Inbred C57BLAcyltransferasesAdaptor Proteins, Signal TransducingAntiviral AgentsDNADoxorubicinInterferon Regulatory Factor-3IRF3 protein, humanLATS1 protein, humanLATS2 protein, humanLysineNucleic AcidsPhosphoproteinsProtein Serine-Threonine KinasesRNATAFAZZIN protein, humanTBK1 protein, humanTranscription FactorsTumor Suppressor ProteinsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID28346439
PMCPMC5398908
OpenAlexW2597511687

What OpenQuestion holds

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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.