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

Rescue of functional DeltaF508-CFTR channels by co-expression with truncated CFTR constructs in COS-1 cells.

FEBS letters - 6 Nov 2003

Owsianik Grzegorz, Cao Lishuang, Nilius Bernd

Abstract excerpt

The most frequent mutant variant of the cystic fibrosis transmembrane conductance regulator (CFTR), DeltaF508-CFTR, is misprocessed and subsequently degraded in the endoplasmic reticulum. Using the patch-clamp technique, we showed that co-expressions of DeltaF508-CFTR with the N-terminal CFTR truncates containing bi-arginine (RXR) retention/retrieval motifs result in a functional rescue of the DeltaF508-CFTR...

Read the complete abstract on PubMed

Topics

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

Share to Chlorides
Share to Cyclic AMP
Share to Cystic Fibrosis Transmembrane Conductance Regulator

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Electrophysiology

Share to Endoplasmic Reticulum

Share to Genetic Therapy

Share to Patch-Clamp Techniques

Share to Protein Engineering

Source

Identifiers

PMID: 14596935
DOI: 10.1016/s0014-5793(03)01162-1

Genes

CFTR

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

Rescue of functional DeltaF508-CFTR channels by co-expression with truncated CFTR constructs in COS-1 cells.PMID 14596935Read ↗

Pharmacological chaperone-rescued cystic fibrosis CFTR-F508del mutant overcomes PRAF2-gated access to endoplasmic reticulum exit sites.Semantic proximity Read ↗

F508del CFTR with two altered RXR motifs escapes from ER quality control but its channel activity is thermally sensitive.Semantic proximity Read ↗

Revisiting CFTR Interactions: Old Partners and New Players.Semantic proximity Read ↗

Generation of ΔF508-CFTR T84 cell lines by CRISPR/Cas9-mediated genome editing.Semantic proximity Read ↗

Full Rescue of F508del-CFTR Processing and Function by CFTR Modulators Can Be Achieved by Removal of Two Regulatory Regions.Semantic proximity Read ↗

The ΔF508-CFTR mutation inhibits wild-type CFTR processing and function when co-expressed in human airway epithelia and in mouse nasal mucosa.Semantic proximity Read ↗

Removal of multiple arginine-framed trafficking signals overcomes misprocessing of delta F508 CFTR present in most patients with cystic fibrosis.Semantic proximity Read ↗

Rescue of F508del CFTR: Commentary on "F508del CFTR with two altered RXR motifs escapes from ER quality control but its channel activity is thermally sensitive".Semantic proximity Read ↗

CFTR folding and maturation in cells.Semantic proximity Read ↗

Control of cystic fibrosis transmembrane conductance regulator membrane trafficking: not just from the endoplasmic reticulum to the Golgi.Semantic proximity Read ↗

Combination of Correctors Rescue ΔF508-CFTR by Reducing Its Association with Hsp40 and Hsp27.Semantic proximity Read ↗

Rescuing cystic fibrosis transmembrane conductance regulator (CFTR)-processing mutants by transcomplementation.Semantic proximity Read ↗

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