Evidence map›Paper›PMID 30533546›Full record

ArticleHeliyon2018

IL-33 suppresses GSK-3β activation through an ST2-independent MyD88/TRAF6/RIP/PI3K/Akt pathway.

Tomoyuki Nishizaki

Abstract read
In one paragraph

Article in Heliyon, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Roles of Cytokines in Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. The IL-33/ST2 Pathway in Cerebral Malaria.International journal of molecular sciences · 2022
    Review
  12. Potential bioactive compounds and mechanisms ofFrontiers in aging neuroscience · 2022
    Article
  13. Article
  14. Article
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

1 author.

Tomoyuki NishizakiShanghai University of Traditional Chinese Medicine, Education College of Medicine, Osaka, 530-0047, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe present study was conducted to explore the effect of interleukin-33 (IL-33) on glycogen synthase kinase-3β (GSK-3β) activation involving Tau phosphorylation, a critical causative factor for Alzheimer's disease (AD). MAIN

methodsExperiments were performed using PC-12 cells. Target proteins were knocked-down by transfecting with the siRNA for each protein. The kinase activities were assessed by monitoring phosphorylation of Thr308 and Ser473 for Akt and phosphorylation of Ser9 and Tyr216 for GSK-3β in the Western blotting. KEY

findingsExogenously applied IL-33 activated Akt and inactivated GSK-3β. IL-33-induced Akt activation and GSK-3β inactivation were significantly inhibited by knocking-down myeloid differentiation factor 88 (MyD88), tumor necrosis factor receptor associated factor 6 (TRAF6), receptor-interacting protein (RIP), or phosphatidylinositol 3 kinase (PI3K). IL-33 neutralized amyloid β SIGNIFICANCE: The results of the present study show that IL-33 inactivates GSK-3β through an ST2-independent MyD88/TRAF6/RIP/PI3K/Akt pathway and inhibits Aβ

Indexed as

Biochemistry

Identifiers

PMID30533546
PMCPMC6260469

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.