Evidence map›Paper›PMID 30107029›Full record

ArticleBritish journal of pharmacology2018

Potentiation of the cystic fibrosis transmembrane conductance regulator by VX-770 involves stabilization of the pre-hydrolytic, O

Emily Langron, Stella Prins, Paola Vergani

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. VX-770, CInternational journal of molecular sciences · 2025
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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 1 institution in 1 country.

Emily LangronNeuroscience, Physiology and Pharmacology, University College London, London, UK.ORCID 0000-0001-7183-7383
Stella PrinsNeuroscience, Physiology and Pharmacology, University College London, London, UK.
Paola VerganiNeuroscience, Physiology and Pharmacology, University College London, London, UK.ORCID 0000-0002-5422-4662
University College London · GB

Funding

Medical Research Council G0501200
6 · The paper itself

Abstract

background and purposeCystic fibrosis (CF) is a debilitating hereditary disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes an anion channel. Wild type-CFTR gating is a non-equilibrium process. After ATP binding, CFTR enters a stable open state (O EXPERIMENTAL APPROACH: Potentiation by VX-770 was measured using microscopic imaging of HEK293 cells expressing an anion-sensitive YFP-CFTR. A simple mathematical model was used to predict fluorescence quenching following extracellular iodide addition and estimate CFTR conductance. Membrane density of CFTR channels was measured in a parallel assay, using CFTR-pHTomato. KEY

resultsVX-770 strongly potentiated WT-CFTR, D1370N-CFTR and K1250R-CFTR. K464A-CFTR was also strongly potentiated, regardless of whether it retained catalytic activity or not. CONCLUSIONS AND IMPLICATIONS: Similar potentiation of hydrolytic and non-hydrolytic mutants suggests that VX-770 increases CFTR open probability mainly by stabilizing pre-hydrolytic O

Indexed as

AminophenolsChloride Channel AgonistsCystic Fibrosis Transmembrane Conductance RegulatorHEK293 CellsHumansHydrolysisIon Channel GatingOptical ImagingQuinolonesAminophenolsCFTR protein, humanChloride Channel AgonistsCystic Fibrosis Transmembrane Conductance RegulatorivacaftorQuinolones

Identifiers

PMID30107029
PMCPMC6151340
OpenAlexW2887380154

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.