ReviewExpert review of proteomics2010
Targets for cystic fibrosis therapy: proteomic analysis and correction of mutant cystic fibrosis transmembrane conductance regulator.
Review in Expert review of proteomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Development of an automated system to measure ion channel currents using a surface-modified gold probe.Scientific reports · 2021Article
- A Lipid Bilayer Formed on a Hydrogel Bead for Single Ion Channel Recordings.Micromachines · 2020Article
- Revisiting Cell Death Responses in Fibrotic Lung Disease: Crosstalk between Structured and Non-Structured Cells.Diagnostics (Basel, Switzerland) · 2020Review
- Recent Progress in CFTR Interactome Mapping and Its Importance for Cystic Fibrosis.Frontiers in pharmacology · 2017Review
- Ribosomal Stalk Protein Silencing Partially Corrects the ΔF508-CFTR Functional Expression Defect.PLoS biology · 2016Article
- Creation and characterization of an airway epithelial cell line for stable expression of CFTR variants.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2016Article
- CFTR Deletion in Mouse Testis Induces VDAC1 Mediated Inflammatory Pathway Critical for Spermatogenesis.PloS one · 2016Article
- ΔF508 CFTR surface stability is regulated by DAB2 and CHIP-mediated ubiquitination in post-endocytic compartments.PloS one · 2015Article
- Genetics of acute and chronic pancreatitis.Current opinion in gastroenterology · 2013Review
- A yeast phenomic model for the gene interaction network modulating CFTR-ΔF508 protein biogenesis.Genome medicine · 2012Article
- Omics approaches in cystic fibrosis research: a focus on oxylipin profiling in airway secretions.Annals of the New York Academy of Sciences · 2012Review
- Metabolomic profiling of regulatory lipid mediators in sputum from adult cystic fibrosis patients.Free radical biology & medicine · 2012Article
- Understanding protein kinase CK2 mis-regulation upon F508del CFTR expression.Naunyn-Schmiedeberg's archives of pharmacology · 2011Review
- Genetics of pancreatitis.Current opinion in gastroenterology · 2011Review
- CFTR expression regulation by the unfolded protein response.Methods in enzymology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Proteomic analysis has proved to be an important tool for understanding the complex nature of genetic disorders, such as cystic fibrosis (CF), by defining the cellular protein environment (proteome) associated with wild-type and mutant proteins. Proteomic screens identified the proteome of CF transmembrane conductance regulator (CFTR), and provided fundamental information to studies designed for understanding the crucial components of physiological CFTR function. Simultaneously, high-throughput screens for small-molecular correctors of CFTR mutants provided promising candidates for therapy. The majority of CF cases are caused by nucleotide deletions (DeltaF508 CFTR; >75%), resulting in CFTR misfolding, or insertion of premature termination codons ( approximately 10%), leading to unstable mRNA and reduced levels of truncated dysfunctional CFTR. In this article, we review recent results of proteomic screens, developments in identifying correctors for the most frequent CFTR mutants, and comment on how integration of the knowledge gained from these studies may aid in finding a cure for CF and a number of other genetic disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.