Evidence map›Paper›PMID 18255040›Full record

ArticleBiochimica et biophysica acta2008

CFTR in a lipid raft-TNFR1 complex modulates gap junctional intercellular communication and IL-8 secretion.

Tecla Dudez, Florence Borot, Song Huang, Brenda R Kwak, Marc Bacchetta, Mario Ollero, Bruce A Stanton, Marc Chanson

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.6field-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

36 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  7. Review
  8. Review
  9. Article
  10. Cyclodextrins reduce the ability of Pseudomonas aeruginosa outer-membrane vesicles to reduce CFTR ClAmerican journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  11. Article
  12. Cerebral artery myogenic reactivity: The next frontier in developing effective interventions for subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Oxidative stress-induced autophagy: role in pulmonary toxicity.Toxicology and applied pharmacology · 2014
    Review
  19. Article
  20. 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

8 authors at 3 institutions in 3 countries.

Tecla DudezLaboratory of Clinical Investigation III, Micheli-du-Crest, Geneva, Switzerland.
Florence Borot
Song Huang
Brenda R Kwak
Marc Bacchetta
Mario Ollero
Bruce A Stanton
Marc Chanson
Inserm · FRUniversity Hospital of Geneva · CHDartmouth College · US

Funding

TRANSLATIONAL RESEARCH COREP30GM106394 · NIGMS · DARTMOUTH COLLEGE · PI MADDEN, DEAN R · 2013 to 2017
$6.1M
Role of Virulence Factors in Pseudomonas-Host InteractionsR01HL074175 · NHLBI · DARTMOUTH COLLEGE · PI STANTON, BRUCE A. · 2003 to 2018
$5.0M
REGULATION OF CFTR TRAFFICKINGR01DK045881 · NIDDK · DARTMOUTH COLLEGE · PI STANTON, BRUCE A. · 1992 to 2008
$2.5M
Cellular and Molecular Mechanisms of Lung DiseaseP20GM103413 · NIGMS · DARTMOUTH COLLEGE · PI STANTON, BRUCE A. · 2012 to 2012
$2.1M
NHLBI NIH HHS R01 HL074175NIDDK NIH HHS DK 045881NIDDK NIH HHS R01 DK045881NIGMS NIH HHS P20 GM103413NIGMS NIH HHS P30 GM106394
6 · The paper itself

Abstract

Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause a chronic inflammatory response in the lung of patients with Cystic Fibrosis (CF). We have showed that TNF-alpha signaling through the Src family tyrosine kinases (SFKs) was defective as determined by an inability of TNF-alpha to regulate gap junctional communication (GJIC) in CF cells. Here, we sought to elucidate the mechanisms linking TNF-alpha signaling to the functions of CFTR at the molecular level. In a MDCKI epithelial cell model expressing wild-type (WtCFTR) or mutant CFTR lacking its PDZ-interacting motif (CFTR-DeltaTRL), TNF-alpha increased the amount of WtCFTR but not CFTR-DeltaTRL in detergent-resistant membrane microdomains (DRMs). This recruitment was modulated by SFK activity and associated with DRM localization of TNFR1 and c-Src. Activation of TNFR1 signaling also decreased GJIC and markedly stimulated IL-8 production in WtCFTR cells. In contrast, the absence of CFTR in DRMs was associated with abnormal TNFR1 signaling as revealed by no recruitment of TNFR1 and c-Src to lipid rafts in CFTR-DeltaTRL cells and loss of regulation of GJIC and IL-8 secretion. These results suggest that localization of CFTR in lipid rafts in association with c-Src and TNFR1 provides a responsive signaling complex to regulate GJIC and cytokine signaling.

Indexed as

Cell CommunicationAnimalsCell LineConnexin 43Cystic Fibrosis Transmembrane Conductance RegulatorDogsGap JunctionsInterleukin-8Membrane MicrodomainsMembrane ProteinsProto-Oncogene Proteins pp60(c-src)Receptors, Tumor Necrosis Factor, Type ISequence DeletionSignal Transductionsrc-Family KinasesTumor Necrosis Factor-alphaConnexin 43Cystic Fibrosis Transmembrane Conductance RegulatorInterleukin-8Membrane ProteinsProto-Oncogene Proteins pp60(c-src)Receptors, Tumor Necrosis Factor, Type Isrc-Family KinasesTumor Necrosis Factor-alpha

Identifiers

PMID18255040
PMCPMC5512004
OpenAlexW2111250302

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.