Evidence map›Paper›PMID 11309505›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2001

Defective regulatory volume decrease in human cystic fibrosis tracheal cells because of altered regulation of intermediate conductance Ca2+-dependent potassium channels.

E Vázquez, M Nobles, M A Valverde

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. LRRC8A-containing chloride channel is crucial for cell volume recovery and survival under hypertonic conditions.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  5. Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Non-essential contribution of LRRC8A to volume regulation.Pflugers Archiv : European journal of physiology · 2016
    Article
  11. Mechanosensitivity of wild-type and G551D cystic fibrosis transmembrane conductance regulator (CFTR) controls regulatory volume decrease in simple epithelia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Mechanosensitive gating of CFTR.Nature cell biology · 2010
    Article
  16. The progesterone receptor regulates the expression of TRPV4 channel.Pflugers Archiv : European journal of physiology · 2009
    Article
  17. Article
  18. Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

E VázquezUnitat de Senyalització Cel.lular, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, C/Dr. Aiguader 80, 08003 Barcelona, Spain.
M Nobles
M A Valverde
Medical Research Council · GBPompeu Fabra University · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cystic fibrosis transmembrane conductance regulator (CFTR) protein has the ability to function as both a chloride channel and a channel regulator. The loss of these functions explains many of the manifestations of the cystic fibrosis disease (CF), including lung and pancreatic failure, meconium ileus, and male infertility. CFTR has previously been implicated in the cell regulatory volume decrease (RVD) response after hypotonic shocks in murine small intestine crypts, an effect associated to the dysfunction of an unknown swelling-activated potassium conductance. In the present study, we investigated the RVD response in human tracheal CF epithelium and the nature of the volume-sensitive potassium channel affected. Neither the human tracheal cell line CFT1, expressing the mutant CFTR-DeltaF508 gene, nor the isogenic vector control line CFT1-LC3, engineered to express the betagal gene, showed RVD. On the other hand, the cell line CFT1-LCFSN, engineered to express the wild-type CFTR gene, presented a full RVD. Patch-clamp studies of swelling-activated potassium currents in the three cell lines revealed that all of them possess a potassium current with the biophysical and pharmacological fingerprints of the intermediate conductance Ca(2+)-dependent potassium channel (IK, also known as KCNN4). However, only CFT1-LCFSN cells showed an increase in IK currents in response to hypotonic challenges. Although the identification of the molecular mechanism relating CFTR to the hIK channel remains to be solved, these data offer new evidence on the complex integration of CFTR in the cells where it is expressed.

Indexed as

Potassium Channels, Calcium-ActivatedCalciumCell LineCell SizeCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorElectric ConductivityHumansHypotonic SolutionsIntermediate-Conductance Calcium-Activated Potassium ChannelsIon TransportPhenotypePotassiumPotassium Channel BlockersPotassium ChannelsTracheaCalciumCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorHypotonic SolutionsIntermediate-Conductance Calcium-Activated Potassium ChannelsKCNN4 protein, humanPotassiumPotassium Channel BlockersPotassium ChannelsPotassium Channels, Calcium-Activated

Identifiers

PMID11309505
PMCPMC33209
OpenAlexW2035386070

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.