ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Airway Epithelial KIF3A Regulates Th2 Responses to Aeroallergens.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis 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
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Skin depletion of Kif3a resembles the pediatric atopic dermatitis transcriptome profile.Human molecular genetics · 2022Pooled it
- Identification of two early life eczema and non-eczema phenotypes with high risk for asthma development.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Trial
- Article
- Role of microRNAs in immunoregulatory functions of epithelial cells.BMC immunology · 2024Review
- How early life respiratory viral infections impact airway epithelial development and may lead to asthma.Frontiers in pediatrics · 2024Review
- A scoping review: What are the cellular mechanisms that drive the allergic inflammatory response to fungal allergens in the lung epithelium?Clinical and translational allergy · 2023Article
- Kinesins in Mammalian Spermatogenesis and Germ Cell Transport.Frontiers in cell and developmental biology · 2022Review
- Disease-associated KIF3A variants alter gene methylation and expression impacting skin barrier and atopic dermatitis risk.Nature communications · 2020Article
- MicroRNA-145-5p promotes asthma pathogenesis by inhibiting kinesin family member 3A expression in mouse airway epithelial cells.The Journal of international medical research · 2019Article
- Kinesin family member 3A induces related diseases via wingless-related integration site/β-catenin signaling pathway.Science progressReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
KIF3A, the gene encoding kinesin family member 3A, is a susceptibility gene locus associated with asthma; however, mechanisms by which KIF3A might influence the pathogenesis of the disorder are unknown. In this study, we deleted the mouse Kif3a gene in airway epithelial cells. Both homozygous and heterozygous Kif3a gene-deleted mice were highly susceptible to aeroallergens from Aspergillus fumigatus and the house dust mite, resulting in an asthma-like pathology characterized by increased goblet cell metaplasia, airway hyperresponsiveness, and Th2-mediated inflammation. Deletion of the Kif3a gene increased the severity of pulmonary eosinophilic inflammation and expression of cytokines (Il-4, Il-13, and Il-17a) and chemokine (Ccl11) RNAs following pulmonary exposure to Aspergillus extract. Inhibition of Kif3a disrupted the structure of motile cilia and impaired mucociliary clearance, barrier function, and epithelial repair, demonstrating additional mechanisms by which deficiency of KIF3A in respiratory epithelial cells contributes to pulmonary pathology. Airway epithelial KIF3A suppresses Th2 pulmonary inflammation and airway hyperresponsiveness following aeroallergen exposure, implicating epithelial microtubular functions in the pathogenesis of Th2-mediated lung pathology.
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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.