Evidence map›Paper›PMID 31139191›Full record

ArticleFrontiers in immunology2019

Mitochondrial Protein PINK1 Positively Regulates RLR Signaling.

Jun Zhou, Rui Yang, Zhaoru Zhang, Qianru Liu, Yuanyuan Zhang, Qingqing Wang, Hongbin Yuan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  6. Pink1 deficiency enhances neurological deficits and inflammatory responses after intracerebral hemorrhage in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Article
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  9. Review
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  15. Review
  16. The Functional Deubiquitinating Enzymes in Control of Innate Antiviral Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Review
  17. PINK1: Multiple mechanisms of neuroprotection.International review of movement disorders · 2021
    Article
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  20. Review
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

7 authors at 4 institutions in 1 country.

Jun ZhouDepartment of Cell Biology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, China.
Rui YangDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Zhaoru ZhangDepartment of Cell Biology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, China.
Qianru LiuDepartment of Cell Biology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, China.
Yuanyuan ZhangThe Children's Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.
Hongbin YuanDepartment of Anesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Zhejiang University · CNSecond Military Medical University · CNChildren's Hospital of Zhejiang University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The serine/threonine kinase phosphatase and tensin homolog (PTEN)-induced putative kinase 1(PINK1) controls mitochondrial quality and plays a vital role in the pathogenesis of early-onset Parkinson's disease. However, whether PINK1 has functions in innate antiviral immunity is largely unknown. Here, we report that viral infection down regulates PINK1 expression in macrophages. PINK1 knockdown results in decreased cytokine production and attenuated IRF3 and NF-κB activation upon viral infection. PINK1 promotes the retinoic-acid-inducible gene I (RIG-I)-like receptors (RLR)-triggered immune responses in a kinase domain-dependent manner. Furthermore, PINK1 associates with TRAF3 via the kinase domain and inhibits Parkin-mediated TRAF3 K48-linked proteasomal degradation. In addition, PINK1 interacts with Yes-associated protein 1 (YAP1) upon viral infection and impairs YAP1/IRF3 complex formation. Collectively, our results demonstrate that PINK1 positively regulates RIG-I triggered innate immune responses by inhibiting TRAF3 degradation and relieving YAP-mediated inhibition of the cellular antiviral response.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCytokinesDEAD Box Protein 58FemaleHEK293 CellsHumansInfantInterferon Regulatory Factor-3MacrophagesMaleMiceMice, Inbred C57BLMitochondrial ProteinsNF-kappa BProtein KinasesAdaptor Proteins, Signal TransducingCytokinesDdx58 protein, mouseDEAD Box Protein 58Interferon Regulatory Factor-3IRF3 protein, humanMitochondrial ProteinsNF-kappa BProtein KinasesPTEN-Induced Putative KinaseReceptors, ImmunologicRIGI protein, humanTNF Receptor-Associated Factor 3Transcription FactorsYAP1 protein, humanYAP-Signaling Proteinsantiviral immune responseIRF3macrophagesPINKRLRTRAF3ubiquitinationYAP1

Identifiers

PMID31139191
PMCPMC6527598
OpenAlexW2945833225

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.