ArticleEMBO molecular medicine2023
Cingulin regulates hair cell cuticular plate morphology and is required for hearing in human and mouse.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- CASZ1 regulates the maturation of outer hair cells and is required for hearing in mice.iScience · 2026Article
- Tight junction structure, assembly and (dys)function.Nature reviews. Molecular cell biology · 2026Review
- Article
- Study Models for Non-Syndromic Hearing Loss.Cells · 2025Review
- Article
- TNFAIP8L2 maintains hair cell function and regulates age-related hearing loss via mTORC1 signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- A feedback circuitry involving γ-actin, β-actin and nonmuscle myosin-2 A controls tight junction and apical cortex mechanics.Nature communications · 2025Article
- Stub1 promotes degradation of the activated Diaph3: A negative feedback regulatory mechanism of the actin nucleator.The Journal of biological chemistry · 2024Article
- Cingulin-nonmuscle myosin interaction plays a role in epithelial morphogenesis and cingulin nanoscale organization.Journal of cell science · 2024Article
- A short guide to the tight junction.Journal of cell science · 2024Review
- Cingulin regulates hair cell cuticular plate morphology and is required for hearing in human and mouse.EMBO molecular medicine · 2023Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
Cingulin (CGN) is a cytoskeleton-associated protein localized at the apical junctions of epithelial cells. CGN interacts with major cytoskeletal filaments and regulates RhoA activity. However, physiological roles of CGN in development and human diseases are currently unknown. Here, we report a multi-generation family presenting with autosomal dominant non-syndromic hearing loss (ADNSHL) that co-segregates with a CGN heterozygous truncating variant, c.3330delG (p.Leu1110Leufs*17). CGN is normally expressed at the apical cell junctions of the organ of Corti, with enriched localization at hair cell cuticular plates and circumferential belts. In mice, the putative disease-causing mutation results in reduced expression and abnormal subcellular localization of the CGN protein, abolishes its actin polymerization activity, and impairs the normal morphology of hair cell cuticular plates and hair bundles. Hair cell-specific Cgn knockout leads to high-frequency hearing loss. Importantly, Cgn mutation knockin mice display noise-sensitive, progressive hearing loss and outer hair cell degeneration. In summary, we identify CGN c.3330delG as a pathogenic variant for ADNSHL and reveal essential roles of CGN in the maintenance of cochlear hair cell structures and auditory function.
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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.