Evidence map›Paper›PMID 27278076›Full record

ArticleScientific reports2016

The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Uses its C-Terminus to Regulate the A2B Adenosine Receptor.

Michael J Watson, Shernita L Lee, Abigail J Marklew, Rodney C Gilmore, Martina Gentzsch, Maria F Sassano, Michael A Gray, Robert Tarran

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Functional CFTR may be required for Prevotella melaninogenica regulation of epithelial cell defense against Staphylococcus aureus.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026
    Article
  2. Review
  3. Ion channels and actin: A tale of two friends.Histology and histopathology · 2025
    Review
  4. CFTR is required for zinc-mediated antibacterial defense in human macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. CFTR regulates brown adipocyte thermogenesis via the cAMP/PKA signaling pathway.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2023
    Article
  7. CFTR, Cell Junctions and the Cytoskeleton.International journal of molecular sciences · 2022
    Review
  8. Purinergic receptors in airway hydration.Biochemical pharmacology · 2021
    Review
  9. Article
  10. SARS-CoV-2 may hijack GPCR signaling pathways to dysregulate lung ion and fluid transport.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. Article
  12. SPLUNC1 is an allosteric modulator of the epithelial sodium channel.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  13. Article
  14. 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

8 authors at 3 institutions in 2 countries.

Michael J WatsonCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
Shernita L LeeCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
Abigail J MarklewCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
Rodney C GilmoreCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
Martina GentzschCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
Maria F SassanoCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
Michael A GrayInstitute for Cell and Molecular Biosciences, Newcastle University, Newcastle-upon-Tyne, Northumberland, UK.
Robert TarranCystic Fibrosis Center/Marsico Lung Institute, 125 Mason Farm Road, The University of North Carolina, Chapel Hill, NC, 27599-7248, USA.
University of North Carolina at Chapel Hill · USLung Institute · USNewcastle University · GB

Funding

SEEDING POSTDOCTORAL INNOVATORS IN RESEARCH &EDUCATIONK12GM000678 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DONALD T LYSLE, Kathryn Joanna Reissner · 1999 to 2026
$30.9M
Vector CoreP30DK065988 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Martina Gentzsch · 2004 to 2026
$26.5M
SPLUNC1-Derived Peptides as ENaC AntagonistsR01HL108927 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TARRAN, ROBERT · 2012 to 2015
$1.4M
Medical Research CouncilNHLBI NIH HHS R01 HL108927NIDDK NIH HHS P30 DK065988NIGMS NIH HHS K12 GM000678
6 · The paper itself

Abstract

CFTR is an apical membrane anion channel that regulates fluid homeostasis in many organs including the airways, colon, pancreas and sweat glands. In cystic fibrosis, CFTR dysfunction causes significant morbidity/mortality. Whilst CFTR's function as an ion channel has been well described, its ability to regulate other proteins is less understood. We have previously shown that plasma membrane CFTR increases the surface density of the adenosine 2B receptor (A2BR), but not of the β2 adrenergic receptor (β2AR), leading to an enhanced, adenosine-induced cAMP response in the presence of CFTR. In this study, we have found that the C-terminal PDZ-domain of both A2BR and CFTR were crucial for this interaction, and that replacing the C-terminus of A2BR with that of β2AR removed this CFTR-dependency. This observation extended to intact epithelia and disruption of the actin cytoskeleton prevented A2BR-induced but not β2AR-induced airway surface liquid (ASL) secretion. We also found that CFTR expression altered the organization of the actin cytoskeleton and PDZ-binding proteins in both HEK293T cells and in well-differentiated human bronchial epithelia. Furthermore, removal of CFTR's PDZ binding motif (ΔTRL) prevented actin rearrangement, suggesting that CFTR insertion in the plasma membrane results in local reorganization of actin, PDZ binding proteins and certain GPCRs.

Indexed as

Cell LineCell MembraneCyclic AMPCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsEpitheliumHEK293 CellsHumansIon TransportReceptor, Adenosine A2BRespiratory MucosaSignal TransductionCFTR protein, humanCyclic AMPCystic Fibrosis Transmembrane Conductance RegulatorReceptor, Adenosine A2B

Identifiers

PMID27278076
PMCPMC4899698
OpenAlexW2418549236

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.