Evidence map›Paper›PMID 35069570›Full record

ArticleFrontiers in immunology2021

Cleavage-Mediated Regulation of Myd88 Signaling by Inflammasome-Activated Caspase-1.

Monika Avbelj, Iva Hafner-Bratkovič, Duško Lainšček, Mateja Manček-Keber, Tina Tinkara Peternelj, Gabriela Panter, Steven P Treon, Boris Gole, Uroš Potočnik, Roman Jerala

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. International journal of molecular sciences · 2023
    Article
  11. Plants (Basel, Switzerland) · 2022
    Article
  12. 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

10 authors at 4 institutions in 2 countries.

Monika AvbeljDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
Iva Hafner-BratkovičDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
Duško LainščekDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
Mateja Manček-KeberDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
Tina Tinkara PeterneljDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
Gabriela PanterDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
Steven P TreonDana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States.
Boris GoleCentre for Human Molecular Genetics and Pharmacogenomics, Faculty of Medicine, University of Maribor, Maribor, Slovenia.
Uroš PotočnikCentre for Human Molecular Genetics and Pharmacogenomics, Faculty of Medicine, University of Maribor, Maribor, Slovenia.
Roman JeralaDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Ljubljana, Slovenia.
National Institute of Chemistry · SIEN-FIST Centre of Excellence (Slovenia) · SIUniversity of Maribor · SIHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coordination among multiple signaling pathways ensures an appropriate immune response, where a signaling pathway may impair or augment another signaling pathway. Here, we report a negative feedback regulation of signaling through the key innate immune mediator MyD88 by inflammasome-activated caspase-1. NLRP3 inflammasome activation impaired agonist- or infection-induced TLR signaling and cytokine production through the proteolytic cleavage of MyD88 by caspase-1. Site-specific mutagenesis was used to identify caspase-1 cleavage site within MyD88 intermediary segment. Different cleavage site location within MyD88 defined the functional consequences of MyD88 cleavage between mouse and human cells. LPS/monosodium urate-induced mouse inflammation model corroborated the physiological role of this mechanism of regulation, that could be reversed by chemical inhibition of NLRP3. While Toll/interleukin-1 receptor (TIR) domain released by MyD88 cleavage additionally contributed to the inhibition of signaling, Waldenström's macroglobulinemia associated MyD88

Indexed as

Immunity, InnateAnimalsCaspase 1Enzyme ActivationHEK293 CellsHumansInflammasomesMiceMice, KnockoutMyeloid Differentiation Factor 88Signal TransductionTHP-1 CellsCasp1 protein, mouseCaspase 1InflammasomesMYD88 protein, humanMyd88 protein, mouseMyeloid Differentiation Factor 88caspase-1inflammasomesinflammationinnate immunityMyd88regulation

Identifiers

PMID35069570
PMCPMC8767097
OpenAlexW4206783242

What OpenQuestion holds

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LicenceCC BY
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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.