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Article

High-throughput screening identifies FAU protein as a regulator of mutant cystic fibrosis transmembrane conductance regulator channel.

The Journal of biological chemistry - 26 Jan 2018

Tomati Valeria, Pesce Emanuela, Caci Emanuela, Sondo Elvira, Scudieri Paolo, Marini Monica, Amato Felice, Castaldo Giuseppe, Ravazzolo Roberto, Galietta Luis J V, Pedemonte Nicoletta

Abstract excerpt

In cystic fibrosis, deletion of phenylalanine 508 (F508del) in the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel causes misfolding and premature degradation. One possible approach to reducing the detrimental health effects of cystic fibrosis could be the identification of proteins whose suppression rescues F508del-CFTR function in bronchial epithelial cells. However, searches for these...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 29158263
DOI: 10.1074/jbc.M117.816595
PMCID: PMC5787799

Genes

CFTR
FAU
CHD4
MLLT6
PLXNA1
TRIM24
UBA2
UBA52

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

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Research trail→

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High-throughput screening identifies FAU protein as a regulator of mutant cystic fibrosis transmembrane conductance regulator channel.PMID 29158263Read ↗

Transcriptomic and Proteostasis Networks of CFTR and the Development of Small Molecule Modulators for the Treatment of Cystic Fibrosis Lung Disease.Semantic proximity Read ↗

Genetic Inhibition Of The Ubiquitin Ligase Rnf5 Attenuates Phenotypes Associated To F508del Cystic Fibrosis Mutation.Semantic proximity Read ↗

Recent Progress in CFTR Interactome Mapping and Its Importance for Cystic FibrosisSemantic proximity Read ↗

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Targets for cystic fibrosis therapy: proteomic analysis and correction of mutant cystic fibrosis transmembrane conductance regulator.Semantic proximity Read ↗

Integrative bioinformatics approaches to identify novel molecular gene expression signatures and pathways of Cystic Fibrosis (CF)Semantic proximity Read ↗

Small-molecule correctors divert CFTR-F508del from ERAD by stabilizing sequential folding states.Semantic proximity Read ↗

Increasing the Endoplasmic Reticulum Pool of the F508del Allele of the Cystic Fibrosis Transmembrane Conductance Regulator Leads to Greater Folding Correction by Small Molecule Therapeutics.Semantic proximity Read ↗

Small molecule correctors divert CFTR-F508del from ERAD by stabilizing sequential folding statesSemantic proximity Read ↗

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