ReviewAmerican journal of physiology. Lung cellular and molecular physiology2010
A novel approach to analyze gene expression data demonstrates that the DeltaF508 mutation in CFTR downregulates the antigen presentation pathway.
Review in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
What it found
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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
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 26 citations in OpenAlex.
- Integrative genomic meta-analysis reveals novel molecular insights into cystic fibrosis and ΔF508-CFTR rescue.Scientific reports · 2020Pooled it
- Selection of reference genes for quantitative PCR: identifying reference genes for airway epithelial cells exposed toAmerican journal of physiology. Lung cellular and molecular physiology · 2020Pooled it
- Analyzing qPCR data: Better practices to facilitate rigor and reproducibility.Biochemistry and biophysics reports · 2025Article
- Identification of Novel Modifier Genes Associated With Pain in Cystic Fibrosis: An In Silico Gene Discovery.Human mutation · 2025Article
- APPLICATION OF QUANTILE DISCRETIZATION AND BAYESIAN NETWORK ANALYSIS TO PUBLICLY AVAILABLE CYSTIC FIBROSIS DATA SETS.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2024Article
- Effects ofAmerican journal of physiology. Cell physiology · 2017Review
- In silico search for modifier genes associated with pancreatic and liver disease in Cystic Fibrosis.PloS one · 2017Article
- CFTR Controls the Activity of NF-κB by Enhancing the Degradation of TRADD.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2016Article
- Decreased expression of HLA-DQ and HLA-DR on cells of the monocytic lineage in cystic fibrosis.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Changes in transcriptome of native nasal epithelium expressing F508del-CFTR and intersecting data from comparable studies.Respiratory research · 2013Article
- Low sphingosine-1-phosphate impairs lung dendritic cells in cystic fibrosis.American journal of respiratory cell and molecular biology · 2013Article
- Does the F508-CFTR mutation induce a proinflammatory response in human airway epithelial cells?American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Article
- Regulation of the epithelial Na+ channel and airway surface liquid volume by serine proteases.Pflugers Archiv : European journal of physiology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Gene array studies comparing cystic fibrosis (CF) and non-CF genotypes should reveal factors that explain variability in CF lung disease progression, yielding insights that lead to improved CF care. To date, studies have reached conflicting conclusions, perhaps due to experimental differences and divergent statistical approaches. This review aims: 1) to summarize the findings of four recent gene studies comparing CF and non-CF genotypes, and 2) to reanalyze original data using a recently developed statistical approach, with the aim of identifying genes and paths consistently regulated by the CF genotype. We identified four studies evaluating the effect of the DeltaF508-CFTR mutation on human airway epithelial cell gene expression, restricting our investigation to human airway epithelial cell studies whose data were accessible in NCBI's Gene Expression Omnibus or the European Bioinformatic Institute's ArrayExpress. Gene expression patterns showed consistent repression of MHC class I antigen presentation genes in CF human airway epithelia, suggesting a novel mechanistic explanation for poor clearance of viral and bacterial infections by CF patients. We also examined proinflammatory and NF-kappaB genes, whose induction is widely accepted as a hallmark of the CF genotype, but found little evidence of induction, consistent with a recent review (Machen TE, Am J Physiol Cell Physiol 291: C218-C230, 2006.). In conclusion, our analysis suggests that the CF genotype may impair immune function in airway epithelial cells but may not increase inflammation. Additional studies are required to determine whether MHC class I gene repression in CF reduces antigen presentation at the protein level and whether repression impairs immune function.
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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.