Evidence map›Paper›PMID 31509299›Full record

ArticleJournal of leukocyte biology2019

RNF144B inhibits LPS-induced inflammatory responses via binding TBK1.

Zhen Zhang, Luoyan Zhang, Bin Wang, Xiaoxiao Zhu, Lin Zhao, Chu Chu, Qiang Guo, Ran Wei, Xunqiang Yin, Yunhong Zhang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

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  17. Targeting TANK-binding kinase 1 (TBK1) in cancer.Expert opinion on therapeutic targets · 2020
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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

11 authors at 3 institutions in 1 country.

Zhen ZhangLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Luoyan ZhangKey Lab of Plant Stress Research, College of Life Science, Shandong Normal University, Jinan, Shandong, China.
Bin WangDepartment of Peripheral Vascular Surgery, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Xiaoxiao ZhuLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Lin ZhaoLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Chu ChuLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Qiang GuoLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Ran WeiLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Xunqiang YinLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Yunhong ZhangLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Xia LiLaboratory for Molecular Immunology, Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Shandong First Medical University · CNAffiliated Hospital of Shandong University of Traditional Chinese Medicine · CNShandong Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune responses need to be precisely controlled to avoid prolonged inflammation and prevent unwanted damage to the host. Here, we report that RNF144B responded dynamically to LPS stimulation and negatively regulated LPS-induced inflammation. We found that RNF144B interacted with the scaffold/dimerization domain (SDD) of TANK binding kinase 1 (TBK1) through the in between RING (IBR) domain to inhibit its phosphorylation and K63-linked polyubiquitination, which led to TBK1 inactivation, IRF3 dephosphorylation, and IFN-β reduction. RNF144B knockdown with siRNA increased IRF3 activation and IFN-β production in response to LPS stimulation. Our study identifies that RNF144B interaction with TBK1 is sufficient to inactivate TBK1 and delineates a previously unrecognized role for RNF144B in innate immune responses.

Indexed as

BiomarkersDisease SusceptibilityGene ExpressionHEK293 CellsHumansInflammationInterferon-betaInterferon Regulatory Factor-3LipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BProtein BindingProtein Serine-Threonine KinasesUbiquitinationUbiquitin-Protein LigasesBiomarkersInterferon-betaInterferon Regulatory Factor-3IRF3 protein, humanLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BProtein Serine-Threonine KinasesRNF144B protein, humanTBK1 protein, humanUbiquitin-Protein Ligasesinflammatory responsesLPSRNF144BTBK1

Identifiers

PMID31509299
PMCPMC6899866
OpenAlexW2972968306

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.