ArticlePLoS genetics2017
A mutation in Nischarin causes otitis media via LIMK1 and NF-κB pathways.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Identifying chronic obstructive pulmonary disease subtypes using multi-trait genetics.EBioMedicine · 2025Article
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- BA inhibits LPS-stimulated inflammatory response and apoptosis in human middle ear epithelial cells by regulating the Nf-Kb/Iκbα axis.Open life sciences · 2024Article
- Otitis media: recent advances in otitis media vaccine development and model systems.Frontiers in microbiology · 2024Review
- Rilmenidine extends lifespan and healthspan in Caenorhabditis elegans via a nischarin I1-imidazoline receptor.Aging cell · 2023Article
- Low Efficacy of Genetic Tests for the Diagnosis of Primary Lymphedema Prompts Novel Insights into the Underlying Molecular Pathways.International journal of molecular sciences · 2022Article
- Snrpb is required in murine neural crest cells for proper splicing and craniofacial morphogenesis.Disease models & mechanisms · 2022Article
- Review
- The transcriptional landscape of the cultured murine middle ear epithelium in vitro.Biology open · 2021Article
- Association of ISL1 polymorphisms and eosinophilic levels among otitis media patients.Journal of clinical laboratory analysis · 2021Article
- Suppression of lncRNA MALAT1 Reduces LPS- or IL-17A-Induced Inflammatory Response in Human Middle Ear Epithelial Cells via the NF-BioMed research international · 2021Article
- Reverse Phase Protein Array Reveals Correlation of Retinoic Acid Metabolism With Cardiomyopathy in Friedreich's Ataxia.Molecular & cellular proteomics : MCP · 2021Article
- Panel 7 - Pathogenesis of otitis media - a review of the literature between 2015 and 2019.International journal of pediatric otorhinolaryngology · 2020Review
- Panel 2- recent advance in otitis media bioinformatics.International journal of pediatric otorhinolaryngology · 2020Review
- 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
- Mutation inFrontiers in genetics · 2020Article
- TheFrontiers in genetics · 2020Article
- Effects of miR-373 Inhibition on Glioblastoma Growth by Reducing Limk1Journal of immunology research · 2020Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
Otitis media (OM), inflammation of the middle ear (ME), is a common cause of conductive hearing impairment. Despite the importance of the disease, the aetiology of chronic and recurrent forms of middle ear inflammatory disease remains poorly understood. Studies of the human population suggest that there is a significant genetic component predisposing to the development of chronic OM, although the underlying genes are largely unknown. Using N-ethyl-N-nitrosourea mutagenesis we identified a recessive mouse mutant, edison, that spontaneously develops a conductive hearing loss due to chronic OM. The causal mutation was identified as a missense change, L972P, in the Nischarin (NISCH) gene. edison mice develop a serous or granulocytic effusion, increasingly macrophage and neutrophil rich with age, along with a thickened, inflamed mucoperiosteum. We also identified a second hypomorphic allele, V33A, with only modest increases in auditory thresholds and reduced incidence of OM. NISCH interacts with several proteins, including ITGA5 that is thought to have a role in modulating VEGF-induced angiogenesis and vascularization. We identified a significant genetic interaction between Nisch and Itga5; mice heterozygous for Itga5-null and homozygous for edison mutations display a significantly increased penetrance and severity of chronic OM. In order to understand the pathological mechanisms underlying the OM phenotype, we studied interacting partners to NISCH along with downstream signalling molecules in the middle ear epithelia of edison mouse. Our analysis implicates PAK1 and RAC1, and downstream signalling in LIMK1 and NF-κB pathways in the development of chronic OM.
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Registered trials
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