ArticleAmerican journal of respiratory and critical care medicine2016
A Chronic Obstructive Pulmonary Disease Susceptibility Gene, FAM13A, Regulates Protein Stability of β-Catenin.
Article in American journal of respiratory and critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 84 papers, 2 of them syntheses that pooled it.
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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
84 citing papers in PubMed, 2 syntheses or guidelines pooled it, 119 citations in OpenAlex.
- Prenatal Particulate Air Pollution and DNA Methylation in Newborns: An Epigenome-Wide Meta-Analysis.Environmental health perspectives · 2019Pooled it
- Integrative genomics identifies new genes associated with severe COPD and emphysema.Respiratory research · 2018Pooled it
- Functional interactors of three genome-wide association study genes are differentially expressed in severe chronic obstructive pulmonary disease lung tissue.Scientific reports · 2017Trial
- Influence of FAM13A gene polymorphism and serum matrix metalloproteinases 9 and 12 on the phenotypes of chronic obstructive pulmonary disease.BMC pulmonary medicine · 2026Article
- Long isoforms of the COPD risk gene FAM13A orchestrate human lung epithelial development.American journal of respiratory cell and molecular biology · 2026Article
- Functionally informed cis and trans proteome-wide association studies prioritize disease-critical genes.Research square · 2026Article
- Functionally informed cis and trans proteome-wide association studies prioritize disease-critical genes.medRxiv : the preprint server for health sciences · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- Single-cell lung eQTL dataset of Asian never-smokers highlights the roles of alveolar cells in lung cancer etiology.bioRxiv : the preprint server for biology · 2026Article
- The Developmental Origins of Asthma and COPD.Annual review of physiology · 2026Review
- The multifaceted role of FAM13A in pulmonary diseases.Frontiers in genetics · 2026Review
- Trends, cross-country inequalities and risk factors in the global burden of chronic obstructive pulmonary disease mortality, 1990-2021: a secondary data analysis of the Global Burden of Disease Study 2021.Tobacco induced diseases · 2026Article
- FAM13A polymorphism is associated with a usual interstitial pneumonia pattern in patients with systemic sclerosis-associated interstitial lung disease.Rheumatology (Oxford, England) · 2025Article
- Peroxiredoxin 4 as a switch regulating PTEN/AKT axis in alveolar macrophages activation.Signal transduction and targeted therapy · 2025Article
- [Prospects of Smoking Hazards Research Using Lung Organoid].Jugan geon-gang gwa jilbyeong · 2025Review
- Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Particulate matter-induced epigenetic modifications and lung complications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- The FAM13A Long Isoform Regulates Cilia Movement and Coordination in Airway Mucociliary Transport.American journal of respiratory cell and molecular biology · 2024Article
- Design principles and therapeutic applications of novel synthetic WNT signaling agonists.iScience · 2024Review
- Aerobic exercise training engages the canonical wnt pathway to improve pulmonary function and inflammation in COPD.BMC pulmonary medicine · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
Abstract
rationaleA genetic locus within the FAM13A gene has been consistently associated with chronic obstructive pulmonary disease (COPD) in genome-wide association studies. However, the mechanisms by which FAM13A contributes to COPD susceptibility are unknown.
objectivesTo determine the biologic function of FAM13A in human COPD and murine COPD models and discover the molecular mechanism by which FAM13A influences COPD susceptibility.
methodsFam13a null mice (Fam13a(-/-)) were generated and exposed to cigarette smoke. The lung inflammatory response and airspace size were assessed in Fam13a(-/-) and Fam13a(+/+) littermate control mice. Cellular localization of FAM13A protein and mRNA levels of FAM13A in COPD lungs were assessed using immunofluorescence, Western blotting, and reverse transcriptase-polymerase chain reaction, respectively. Immunoprecipitation followed by mass spectrometry identified cellular proteins that interact with FAM13A to reveal insights on FAM13A's function. MEASUREMENTS AND MAIN
resultsIn murine and human lungs, FAM13A is expressed in airway and alveolar type II epithelial cells and macrophages. Fam13a null mice (Fam13a(-/-)) were resistant to chronic cigarette smoke-induced emphysema compared with Fam13a(+/+) mice. In vitro, FAM13A interacts with protein phosphatase 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3β and β-catenin, inducing β-catenin degradation. Fam13a(-/-) mice were also resistant to elastase-induced emphysema, and this resistance was reversed by coadministration of a β-catenin inhibitor, suggesting that FAM13A could increase the susceptibility of mice to emphysema development by inhibiting β-catenin signaling. Moreover, human COPD lungs had decreased protein levels of β-catenin and increased protein levels of FAM13A.
conclusionsWe show that FAM13A may influence COPD susceptibility by promoting β-catenin degradation.
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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.