Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Small-molecule correctors of defective DeltaF508-CFTR cellular processing identified by high-throughput screening.

The Journal of clinical investigation - 1 Sept 2005

Pedemonte Nicoletta, Lukacs Gergely L, Du Kai, Caci Emanuela, Zegarra-Moran Olga, Galietta Luis J V, Verkman A S

Abstract excerpt

The most common cause of cystic fibrosis (CF) is deletion of phenylalanine 508 (DeltaF508) in the CF transmembrane conductance regulator (CFTR) chloride channel. The DeltaF508 mutation produces defects in folding, stability, and channel gating. To identify small-molecule correctors of defective cellular processing, we assayed iodide flux in DeltaF508-CFTR-transfected epithelial cells using a fluorescent halide...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Colforsin
Share to Drug Design

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genistein

Share to Iodides

Share to Luminescent Proteins

Share to Pyrimidinones

Share to Respiratory Mucosa

Share to Thiazoles

Source

Open in PubMed Open full text

Identifiers

PMID: 16127463
DOI: 10.1172/JCI24898
PMCID: PMC1190372

Genes

CFTR

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Small-molecule correctors of defective DeltaF508-CFTR cellular processing identified by high-throughput screening.PMID 16127463Read ↗

Identification of novel F508del-CFTR traffic correctors among triazole derivatives.Semantic proximity Read ↗

A chemical corrector modifies the channel function of F508del-CFTR.Semantic proximity Read ↗

Functional Rescue of F508del-CFTR Using Small Molecule CorrectorsSemantic proximity Read ↗

Rescue of ΔF508-CFTR trafficking and gating in human cystic fibrosis airway primary cultures by small moleculesSemantic proximity Read ↗

Synergy-based small-molecule screen using a human lung epithelial cell line yields ΔF508-CFTR correctors that augment VX-809 maximal efficacy.Semantic proximity Read ↗

CFTR chloride channel drug discovery--inhibitors as antidiarrheals and activators for therapy of cystic fibrosis.Semantic proximity Read ↗

Rescue of the mutant CFTR chloride channel by pharmacological correctors and low temperature analyzed by gene expression profiling.Semantic proximity Read ↗

Translating in vitro CFTR rescue into small molecule correctors for cystic fibrosis using the Library of Integrated Network-based Cellular Signatures drug discovery platform.Semantic proximity Read ↗

High-throughput screening of libraries of compounds to identify CFTR modulators.Semantic proximity Read ↗

Optimization of a Yellow fluorescent protein-based iodide influx high-throughput screening assay for cystic fibrosis transmembrane conductance regulator (CFTR) modulators.Semantic proximity Read ↗

Pharmacological Correctors of Mutant CFTR MistraffickingSemantic proximity Read ↗

Targeting F508del-CFTR to develop rational new therapies for cystic fibrosis.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.