Evidence map›Paper›PMID 25246634›Full record

ArticleMolecular and cellular biology2014

The WNT signaling pathway contributes to dectin-1-dependent inhibition of Toll-like receptor-induced inflammatory signature.

Jamma Trinath, Sahana Holla, Kasturi Mahadik, Praveen Prakhar, Vikas Singh, Kithiganahalli Narayanaswamy Balaji

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.5field-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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. TLR/WNT: A Novel Relationship in Immunomodulation of Lung Cancer.International journal of molecular sciences · 2022
    Review
  9. PARK2 regulates eIF4B-driven lymphomagenesis.Molecular cancer research : MCR · 2022
    Article
  10. Review
  11. Article
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  13. Article
  14. Article
  15. Review
  16. Article
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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

6 authors at 1 institution in 1 country.

Jamma TrinathDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Sahana HollaDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Kasturi MahadikDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Praveen PrakharDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Vikas SinghDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India.
Kithiganahalli Narayanaswamy BalajiDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, Karnataka, India balaji@mcbl.iisc.ernet.in.
Indian Institute of Science Bangalore · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages regulate cell fate decisions during microbial challenges by carefully titrating signaling events activated by innate receptors such as dectin-1 or Toll-like receptors (TLRs). Here, we demonstrate that dectin-1 activation robustly dampens TLR-induced proinflammatory signature in macrophages. Dectin-1 induced the stabilization of β-catenin via spleen tyrosine kinase (Syk)-reactive oxygen species (ROS) signals, contributing to the expression of WNT5A. Subsequently, WNT5A-responsive protein inhibitors of activated STAT (PIAS-1) and suppressor of cytokine signaling 1 (SOCS-1) mediate the downregulation of IRAK-1, IRAK-4, and MyD88, resulting in decreased expression of interleukin 12 (IL-12), IL-1β, and tumor necrosis factor alpha (TNF-α). In vivo activation of dectin-1 with pathogenic fungi or ligand resulted in an increased bacterial burden of Mycobacteria, Klebsiella, Staphylococcus, or Escherichia, with a concomitant decrease in TLR-triggered proinflammatory cytokines. All together, our study establishes a new role for dectin-1-responsive inhibitory mechanisms employed by virulent fungi to limit the proinflammatory environment of the host.

Indexed as

AnimalsAspergillus flavusAspergillus fumigatusBacterial Loadbeta CateninCandida albicansDectin-1Down-RegulationEnzyme ActivationEscherichiaInflammationInterleukin-12Interleukin-1betaInterleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsKlebsiellabeta CateninDectin-1IL1B protein, mouseInterleukin-12Interleukin-1betaInterleukin-1 Receptor-Associated KinasesIntracellular Signaling Peptides and ProteinsIrak1 protein, mouseIrak4 protein, mouseLectins, C-TypeMyd88 protein, mouseMyeloid Differentiation Factor 88Pias1 protein, mouseProtein Inhibitors of Activated STATProtein-Tyrosine KinasesReactive Oxygen SpeciesSocs1 protein, mouseSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsSyk KinaseSyk protein, mouseToll-Like ReceptorsTumor Necrosis Factor-alphaWnt-5a ProteinWnt5a protein, mouseWnt Proteins

Identifiers

PMID25246634
PMCPMC4248746
OpenAlexW2061460524

What OpenQuestion holds

Textmetadata
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.