Evidence map›Paper›PMID 23072488›Full record

ReviewBritish journal of pharmacology2013

Local modulation of cystic fibrosis conductance regulator: cytoskeleton and compartmentalized cAMP signalling.

Stefania Monterisi, Valeria Casavola, Manuela Zaccolo

Abstract readReview
In one paragraph

Review in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  2. Review
  3. CFTR, Cell Junctions and the Cytoskeleton.International journal of molecular sciences · 2022
    Review
  4. Dysregulation of ion transport in the lung epithelium infected with SARS-CoV-2.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  5. 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
  6. Article
  7. Article
  8. CFTR channel in oocytes from Xenopus laevis and its regulation by xShroom1 protein.Pflugers Archiv : European journal of physiology · 2016
    Article
  9. Article
  10. Article
  11. CFTR and sphingolipids mediate hypoxic pulmonary vasoconstriction.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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.

Stefania MonterisiDepartment of Physiology, Anatomy and Genetics, Oxford University, Oxford, UK.
Valeria Casavola
Manuela Zaccolo

Funding

CRCNS: Spatial & Temporal Aspects of cAMP/PKA Signaling Underlying InformationR01AA018060 · NIAAA · GEORGE MASON UNIVERSITY · PI ABEL, EDWIN TED G., BLACKWELL, KIM L · 2008 to 2012
$1.8M
British Heart FoundationNIAAA NIH HHS IH R01 AA18060NIAAA NIH HHS R01 AA018060
6 · The paper itself

Abstract

The cystic fibrosis conductance regulator (CFTR) is a cAMP-regulated Cl(-) channel expressed predominantly at the apical membrane of secreting epithelial cells. Mutations in the CFTR gene lead to cystic fibrosis, the most frequent genetic disease in the Caucasian population. The most common mutation, a deletion of phenylalanine at position 508 (F508del), impairs CFTR folding and chloride channel function. Although an intense effort is under way to identify compounds that target the F508del CFTR structural defect and promote its expression and stability at the plasma membrane, so far their clinical efficacy has proven to be poor, highlighting the necessity to better understand the molecular mechanism of CFTR regulation and of the pathogenesis of the disease. Accumulating evidence suggests that the inclusion of the CFTR in macromolecular complexes and its interaction with the cortical cytoskeleton may play a key role in fine-tuning the regulation of channel function. Here we review some recent findings that support a critical role for protein-protein interactions involving CFTR and for the cytoskeleton in promoting local control of channel activity. These findings indicate that compounds that rescue and stabilize CFTR at the apical membrane may not be sufficient to restore its function unless the appropriate intracellular milieu is also reconstituted.

Indexed as

AnimalsChloride ChannelsCyclic AMPCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorCytoskeletonDrug DesignEpithelial CellsHumansMolecular Targeted TherapyMutationSignal TransductionChloride ChannelsCyclic AMPCystic Fibrosis Transmembrane Conductance Regulator

Identifiers

PMID23072488
PMCPMC3632233

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.