ArticleHearing research2013
A new Atp2b2 deafwaddler allele, dfw(i5), interacts strongly with Cdh23 and other auditory modifiers.
Article in Hearing research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 22 citations in OpenAlex.
- CaProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Machine learning-based gait classification and genome-wide association identify a QTL for gait type in Colombian paso horses.iScience · 2026Article
- The Role of Calcium Signaling in Sensorineural Hearing Loss.International journal of medical sciences · 2025Review
- Deafness causing neuroplastin missense variants fail to promote plasma membrane CaThe Journal of biological chemistry · 2024Article
- Absence of Embigin accelerates hearing loss and causes sub-viability, brain and heart defects in C57BL/6N mice due to interaction withiScience · 2023Article
- Collapsin Response Mediator Protein 1 (CRMP1) Is Required for High-Frequency Hearing.The American journal of pathology · 2022Article
- Identification and characterisation of spontaneous mutations causing deafness from a targeted knockout programme.BMC biology · 2022Article
- RIBEYE B-Domain Is Essential for RIBEYE A-Domain Stability and Assembly of Synaptic Ribbons.Frontiers in molecular neuroscience · 2022Article
- Neuroplastin genetically interacts with Cadherin 23 and the encoded isoform Np55 is sufficient for cochlear hair cell function and hearing.PLoS genetics · 2022Article
- Rbm24 regulates inner-ear-specific alternative splicing and is essential for maintaining auditory and motor coordination.RNA biology · 2021Article
- Tonotopy in calcium homeostasis and vulnerability of cochlear hair cells.Hearing research · 2019Review
- De novo and inherited loss-of-function variants of ATP2B2 are associated with rapidly progressive hearing impairment.Human genetics · 2019Article
- Early growth response protein 1 regulates promoter activity of α-plasma membrane calcium ATPase 2, a major calcium pump in the brain and auditory system.BMC molecular biology · 2017Article
- Changes in cochlear PMCA2 expression correlate with the maturation of auditory sensitivity.Journal of the Association for Research in Otolaryngology : JARO · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tight regulation of calcium (Ca2+) concentrations in the stereocilia bundles of auditory hair cells of the inner ear is critical to normal auditory transduction. The plasma membrane Ca2+ ATPase 2 (PMCA2), encoded by the Atp2b2 gene, is the primary mechanism for clearance of Ca2+ from auditory stereocilia, keeping intracellular levels low, and also contributes to maintaining adequate levels of extracellular Ca2+ in the endolymph. This study characterizes a novel null Atp2b2 allele, dfw(i5), by examining cochlear anatomy, vestibular function and auditory physiology in mutant mice. Loss of auditory function in PMCA2 mutants can be attributed to dysregulation of intracellular Ca2+ inside the stereocilia bundles. However, extracellular Ca2+ ions surrounding the stereocilia are also required for rigidity of cadherin 23, a component of the stereocilia tip-link encoded by the Cdh23 gene. This study further resolves the interaction between Atp2b2 and Cdh23 in a gene dosage and frequency-dependent manner, and finds that low frequencies are significantly affected by the interaction. In +/dfw(i5) mice, one mutant copy of Cdh23 is sufficient to cause broad frequency hearing impairment. Additionally, we report another modifying interaction with Atp2b2 on auditory sensitivity, possibly caused by an unidentified hearing loss gene in mice.
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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.