ArticlePhysiological genomics2006
Genetic segregation of airway disease traits despite redundancy of calcium-activated chloride channel family members.
Article in Physiological genomics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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.
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Who cites it
54 citing papers in PubMed, 71 citations in OpenAlex.
- MAPK13 controls structural remodeling and disease after epithelial injury.bioRxiv : the preprint server for biology · 2024Article
- Mitogen-activated protein kinase-guided drug discovery for post-viral and related types of lung disease.European respiratory review : an official journal of the European Respiratory Society · 2024Article
- A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A potent MAPK13-14 inhibitor prevents airway inflammation and mucus production.bioRxiv : the preprint server for biology · 2023Article
- Chloride channel accessory 1 gene deficiency causes selective loss of mucus production in a new pig model.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Age-Dependent Reduction in Asthmatic Pathology through Reprogramming of Postviral Inflammatory Responses.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
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- Basal epithelial stem cells cross an alarmin checkpoint for postviral lung disease.The Journal of clinical investigation · 2021Article
- CLCA1 Regulates Airway Mucus Production and Ion Secretion Through TMEM16A.International journal of molecular sciences · 2021Article
- TLR3-Activated Monocyte-Derived Dendritic Cells Trigger Progression from Acute Viral Infection to Chronic Disease in the Lung.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Inducible epithelial resistance against acute Sendai virus infection prevents chronic asthma-like lung disease in mice.British journal of pharmacology · 2020Article
- Calcium-activated chloride channel regulator 1 (CLCA1) forms non-covalent oligomers in colonic mucus and has mucin 2-processing properties.The Journal of biological chemistry · 2019Article
- Respiratory Enterovirus (like Parainfluenza Virus) Can Cause Chronic Lung Disease if Protection by Airway Epithelial STAT1 Is Lost.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Epithelial-Immune Cell Interactions for Drug Discovery in Chronic Obstructive Pulmonary Disease.Annals of the American Thoracic Society · 2018Review
- Influenza A Virus Infection Causes Chronic Lung Disease Linked to Sites of Active Viral RNA Remnants.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Calcium-activated Chloride Channel Regulator 1 (CLCA1) Controls Mucus Expansion in Colon by Proteolytic Activity.EBioMedicine · 2018Article
- Soluble mucus component CLCA1 modulates expression of leukotactic cytokines and BPIFA1 in murine alveolar macrophages but not in bone marrow-derived macrophages.Histochemistry and cell biology · 2018Article
- Article
- Modulation of TMEM16A channel activity by the von Willebrand factor type A (VWA) domain of the calcium-activated chloride channel regulator 1 (CLCA1).The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Complex airway diseases such as asthma and chronic obstructive pulmonary disease exhibit stereotyped traits (especially airway hyperreactivity and mucous cell metaplasia) that are variably expressed in each patient. Here, we used a mouse model for virus-induced long-term expression of these traits to determine whether individual traits can be genetically segregated and thereby linked to separate determinants. We showed that an F2 intercross population derived from susceptible and nonsusceptible mouse strains can manifest individual phenotypic extremes that exhibit one or the other disease trait. Functional genomic analysis of these extremes further indicated that a member of the calcium-activated chloride channel (CLCA) gene family designated mClca3 was inducible with mucous cell metaplasia but not airway hyperreactivity. In confirmation of this finding, we found that mClca3 gene transfer to mouse airway epithelium was sufficient to induce mucous cell metaplasia but not airway hyperreactivity. However, newly developed mClca3(-/-) mice exhibited the same degree of mucous cell metaplasia and airway hyperreactivity as wild-type mice. Bioinformatic analysis of the Clca locus led to the identification of mClca5, and gene transfer indicated that mClca5 also selectively drives mucous cell metaplasia. Thus, in addition to the capacity of CLCA family members to exhibit diverse functional activities, there is also preserved function so that more than one family member mediates mucous cell metaplasia. Nonetheless, Clca expression appears to be a selective determinant of mucous cell metaplasia so that shared homologies between CLCA family members may still represent a useful target for focused therapeutic intervention in hypersecretory airway disease.
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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.