ArticleScientific reports2018
Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- The transcriptional landscape of the cultured murine middle ear epithelium in vitro.Biology open · 2021Article
- Panel 1: Biotechnology, biomedical engineering and new models of otitis media.International journal of pediatric otorhinolaryngology · 2020Review
- Panel 3: Genomics, precision medicine and targeted therapies.International journal of pediatric otorhinolaryngology · 2020Review
- Genomics of Otitis Media (OM): Molecular Genetics Approaches to Characterize Disease Pathophysiology.Frontiers in genetics · 2020Review
- Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model.Disease models & mechanisms · 2019Article
- Current Understanding of Host Genetics of Otitis Media.Frontiers in genetics · 2019Review
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Otitis Media (OM) is characterized by epithelial abnormalities and defects in innate immunity in the middle ear (ME). Although, BPIFA1, a member of the BPI fold containing family of putative innate defence proteins is abundantly expressed by the ME epithelium and SNPs in Bpifa1 have been associated with OM susceptibility, its role in the ME is not well characterized. We investigated the role of BPIFA1 in protection of the ME and the development of OM using murine models. Loss of Bpifa1 did not lead to OM development. However, deletion of Bpifa1 in Evi1
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