Evidence map›Paper›PMID 11707576›Full record

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

Compartmentalized autocrine signaling to cystic fibrosis transmembrane conductance regulator at the apical membrane of airway epithelial cells.

P Huang, E R Lazarowski, R Tarran, S L Milgram, R C Boucher, M J Stutts

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 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
17.2field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 203 citations in OpenAlex.

  1. Article
  2. Review
  3. CFTR, Cell Junctions and the Cytoskeleton.International journal of molecular sciences · 2022
    Review
  4. Review
  5. Purinergic receptors in airway hydration.Biochemical pharmacology · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  15. Review
  16. Article
  17. Review
  18. Physiology of epithelial chloride and fluid secretion.Cold Spring Harbor perspectives in medicine · 2012
    Article
  19. Article
  20. Transgenic hCFTR expression fails to correct β-ENaC mouse lung disease.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article

29 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

P HuangCystic Fibrosis Research and Treatment Center, University of North Carolina, Chapel Hill, NC 27599-7248, USA. huangp@med.unc.edu
E R Lazarowski
R Tarran
S L Milgram
R C Boucher
M J Stutts
University of North Carolina at Chapel Hill · USPulmonary Associates · US

Funding

THE BIOLOGY OF MUCUS AND MUCUS PLAQUES ON CF AIRWAYSP50HL060280 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BOUCHER, RICHARD CHARLES · 1998 to 2007
$14.0M
COUPLING OF ADENOSINE RECEPTORS WITH CFTRK01DK002777 · NIDDK · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI HUANG, PINGBO · 2000 to 2002
$244k
NHLBI NIH HHS HL60280-02NHLBI NIH HHS P50 HL060280NIDDK NIH HHS KO1 DK02777-01
6 · The paper itself

Abstract

Physical stimulation of airway surfaces evokes liquid secretion, but the events that mediate this vital protective function are not understood. When cystic fibrosis transmembrane conductance regulator (CFTR) channel activity was used as a functional readout, we found signaling elements compartmentalized at both extracellular and intracellular surfaces of the apical cell membrane that activate apical Cl(-) conductance in Calu-3 cells. At the outer surface, ATP was released by physical stimuli, locally converted to adenosine, and sensed by A(2B) adenosine receptors. These receptors couple to G proteins, adenylyl cyclase, and protein kinase A, at the intracellular face of the apical membrane to activate colocalized CFTR. Thus, airways have evolved highly efficient mechanisms to "flush" noxious stimuli from airway surfaces by selective activation of apical membrane signal transduction and effector systems.

Indexed as

AdenosineAdenosine TriphosphateAdenylyl CyclasesAutocrine CommunicationCell LineCell MembraneChloridesCyclic AMPCyclic AMP-Dependent Protein KinasesCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorElectrophysiologyEpithelial CellsGTP-Binding Protein alpha Subunits, GsGuanosine 5'-O-(3-Thiotriphosphate)HumansAdenosineAdenosine TriphosphateAdenylyl CyclasesCFTR protein, humanChloridesCyclic AMPCyclic AMP-Dependent Protein KinasesCystic Fibrosis Transmembrane Conductance RegulatorGTP-Binding Protein alpha Subunits, GsGuanosine 5'-O-(3-Thiotriphosphate)Receptor, Adenosine A2BReceptors, Purinergic P1

Identifiers

PMID11707576
PMCPMC61178
OpenAlexW2112998606

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.