Evidence map›Paper›PMID 24693944›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

MUC1 regulates epithelial inflammation and apoptosis by PolyI:C through inhibition of Toll/IL-1 receptor-domain-containing adapter-inducing IFN-β (TRIF) recruitment to Toll-like receptor 3.

Kosuke Kato, Erik P Lillehoj, Kwang Chul Kim

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The role of mucin 1 in respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  10. Evodiamine suppresses non-small cell lung cancer by elevating CD8Journal of experimental & clinical cancer research : CR · 2020
    Article
  11. MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Membrane-Tethered MUC1 Mucin Counter-Regulates the Phagocytic Activity of Macrophages.American journal of respiratory cell and molecular biology · 2016
    Article
  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

3 authors at 2 institutions in 1 country.

Kosuke Kato1 Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, Pennsylvania; and.
Erik P Lillehoj
Kwang Chul Kim
Temple University · USUniversity of Maryland, Baltimore · US

Funding

SIGNALING MECHANISM OF MUC1 MUCINR01HL047125 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI KIM, KWANG CHUL · 1991 to 2015
$4.5M
NHLBI NIH HHS HL-47125NHLBI NIH HHS R01 HL047125
6 · The paper itself

Abstract

MUC1/Muc1 (MUC1 in humans, Muc1 in animals) is a membrane-tethered mucin expressed by airway epithelial cells and plays an antiinflammatory role during airway bacterial infection. We previously demonstrated that MUC1/Muc1 is a negative regulator of Toll-like receptor (TLR) inflammatory signaling mediated through the myeloid differentiation primary response gene 88 (MyD88) adaptor protein. In the present study, we determined whether MUC1 regulates MyD88-independent TLR signaling mediated through the TLR3-Toll/IL-1 receptor-domain-containing adapter-inducing IFN-β (TRIF) pathway in response to poly(I:C). Compared with MUC1/Muc1-expressing controls, cells deficient in MUC1/Muc1 were more prone to poly(I:C)-induced apoptosis; had increased poly(I:C)-driven activation of caspase-3, caspase-8, IFN regulatory factor-3, and NF-κB; and displayed heightened IFN-β gene expression. MUC1 overexpression by these cells had the opposite effects. Reciprocal coimmunoprecipitation experiments established constitutive TLR3/MUC1-CT (cytoplasmic tail) protein interaction in human embryonic kidney (HEK)293T cells overexpressing the two proteins and in lung epithelial cells expressing the endogenous proteins, the latter of which was confirmed by immunofluorescence colocalization of TLR3 with MUC1-CT. Coimmunoprecipitation studies also revealed that MUC1 overexpression by HEK293T cells reduced poly(I:C)-induced TLR3/TRIF protein interaction. Finally, MUC1 overexpression had no effect on TRIF-dependent auto-activation of TLR3 signaling, suggesting that the site of action of the MUC1-CT in TLR3 signaling is not downstream of TRIF. These data indicate that MUC1-CT counter-regulates apoptotic and inflammatory responses of airway epithelial cell through constitutive association with TLR3, thereby inhibiting poly(I:C)-induced recruitment of TRIF to TLR3.

Indexed as

ApoptosisAdaptor Proteins, Vesicular TransportCaspase 3Caspase 8Cell Line, TumorEpithelial CellsGene Expression RegulationHEK293 CellsHumansInflammationInterferon Regulatory Factor-3LungMucin-1NF-kappa B p50 SubunitPoly I-CProtein Structure, TertiaryAdaptor Proteins, Vesicular TransportCASP3 protein, humanCASP8 protein, humanCaspase 3Caspase 8Interferon Regulatory Factor-3IRF3 protein, humanMUC1 protein, humanMucin-1NF-kappa B p50 SubunitNFKB1 protein, humanPoly I-CRNA, Small InterferingTICAM1 protein, humanTLR3 protein, humanToll-Like Receptor 3apoptosisMUC1poly(I:C)Toll/IL-1 receptor-domain–containing adapter-inducing IFN-βToll-like receptor 3

Identifiers

PMID24693944
PMCPMC4189494
OpenAlexW2168017635

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.