Evidence map›Paper›PMID 29125880›Full record

ArticlePLoS pathogens2017

MAVS activates TBK1 and IKKε through TRAFs in NEMO dependent and independent manner.

Run Fang, Qifei Jiang, Xiang Zhou, Chenguang Wang, Yukun Guan, Jianli Tao, Jianzhong Xi, Ji-Ming Feng, Zhengfan Jiang

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

134 citing papers in PubMed, 198 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Microbiology spectrum · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Deubiquitinase OTULIN dampens RIG-I-dependent antiviral signaling by removing linear ubiquitination from TRAF6.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  11. N6-methyladenosine modification of FZR1 mRNA positively regulates antiviral innate immunity by targeting the MAVS-TRAF3/6 axis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
  13. Article
  14. Review
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  17. Article
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  19. Article
  20. Review

74 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

9 authors at 2 institutions in 2 countries.

Run FangKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.
Qifei JiangKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.
Xiang ZhouKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.
Chenguang WangKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.
Yukun GuanKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.ORCID http://orcid.org/0000-0001-9312-0164
Jianli TaoKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.ORCID http://orcid.org/0000-0003-0100-1489
Jianzhong XiInstitute of Molecular Medicine, Peking University, Beijing, China.
Ji-Ming FengDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana, United States of America.
Zhengfan JiangKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.ORCID http://orcid.org/0000-0002-1247-1382
Peking University · CNLouisiana State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial antiviral-signaling protein (MAVS) transmits signals from RIG-I-like receptors after RNA virus infections. However, the mechanism by which MAVS activates downstream components, such as TBK1 and IKKα/β, is unclear, although previous work suggests the involvement of NEMO or TBK1-binding proteins TANK, NAP1, and SINTBAD. Here, we report that MAVS-mediated innate immune activation is dependent on TRAFs, partially on NEMO, but not on TBK1-binding proteins. MAVS recruited TBK1/IKKε by TRAFs that were pre-associated with TBK1/IKKε via direct interaction between the coiled-coil domain of TRAFs and the SDD domain of TBK1/IKKε. TRAF2-/-3-/-5-/-6-/- cells completely lost RNA virus responses. TRAFs' E3 ligase activity was required for NEMO activation by synthesizing ubiquitin chains that bound to NEMO for NF-κB and TBK1/IKKε activation. NEMO-activated IKKα/β were important for TBK1/IKKε activation through IKKα/β-mediated TBK1/IKKε phosphorylation. Moreover, individual TRAFs differently mediated TBK1/IKKε activation and thus fine-tuned antiviral immunity under physiological conditions.

Indexed as

Adaptor Proteins, Signal TransducingHEK293 CellsHumansI-kappa B KinaseImmunity, InnatePhosphorylationProtein Serine-Threonine KinasesSendai virusSignal TransductionUbiquitinationAdaptor Proteins, Signal TransducingI-kappa B KinaseIKBKG protein, humanMAVS protein, humanProtein Serine-Threonine Kinases

Identifiers

PMID29125880
PMCPMC5699845
OpenAlexW2767451245

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.