ArticleScientific reports2015
Deletion of Tricellulin Causes Progressive Hearing Loss Associated with Degeneration of Cochlear Hair Cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- A Systematic Review of Genes Affecting Endocochlear Potential.Journal of the Association for Research in Otolaryngology : JARO · 2026Pooled it
- Cis-regulatory evolution reveals sensory trade-offs as a genetic basis for temporal niche evolution in tapirs.Science advances · 2026Article
- Roles of protein-protein interactions and monolayer mechanics in tricellulin localization to tricellular tight junctions.Biology open · 2025Article
- Discovery and mechanism of K63-linkage-directed deubiquitinase activity in USP53.Nature chemical biology · 2025Article
- Bi-AllelicInternational journal of molecular sciences · 2025Article
- Novel compound heterozygous variants in MARVELD2 causing autosomal recessive hearing loss in two Chinese families.Molecular genetics & genomic medicine · 2024Article
- The Basic Requirement of Tight Junction Proteins in Blood-Brain Barrier Function and Their Role in Pathologies.International journal of molecular sciences · 2024Review
- A short guide to the tight junction.Journal of cell science · 2024Review
- Case report: A novel nonsense mutation in theFrontiers in genetics · 2024Article
- Transgenic animal models to explore and modulate the blood brain and blood retinal barriers of the CNS.Fluids and barriers of the CNS · 2022Review
- Angulin-1 seals tricellular contacts independently of tricellulin and claudins.The Journal of cell biology · 2021Article
- Tight Junctions of the Neurovascular Unit.Frontiers in molecular neuroscience · 2021Review
- Tight Junction Modulating Bioprobes for Drug Delivery System to the Brain: A Review.Pharmaceutics · 2020Review
- The Role of Tricellulin in Epithelial Jamming and Unjamming via Segmentation of Tricellular Junctions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- The extracellular domain of angulin-1 and palmitoylation of its cytoplasmic region are required for angulin-1 assembly at tricellular contacts.The Journal of biological chemistry · 2020Article
- Striatin Is Required for Hearing and Affects Inner Hair Cells and Ribbon Synapses.Frontiers in cell and developmental biology · 2020Article
- Tight Junctions in Cell Proliferation.International journal of molecular sciences · 2019Review
- Apoptotic Fragmentation of Tricellulin.International journal of molecular sciences · 2019Article
- ZO-2 Is a Master Regulator of Gene Expression, Cell Proliferation, Cytoarchitecture, and Cell Size.International journal of molecular sciences · 2019Review
- Tricellulin Expression and its Deletion Effects in the Endolymphatic Sac.The journal of international advanced otology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tricellulin (also known as MARVELD2) is considered as a central component of tricellular tight junctions and is distributed among various epithelial tissues. Although mutations in the gene encoding tricellulin are known to cause deafness in humans (DFNB49) and mice, the influence of its systemic deletion in vivo remains unknown. When we generated tricellulin-knockout mice (Tric(-/-)), we found an early-onset rapidly progressive hearing loss associated with the degeneration of hair cells (HCs); however, their body size and overall appearance were normal. Tric(-/-) mice did not show any morphological change pertaining to other organs such as the gastrointestinal tract, liver, kidney, thyroid gland and heart. The endocochlear potential (EP) was normal in Tric(-/-) mice, suggesting that the tight junction barrier is maintained in the stria vascularis, where EP is generated. The degeneration of HCs, which occurred after the maturation of EP, was prevented in the culture medium with an ion concentration similar to that of the perilymph. These data demonstrate the specific requirement of tricellulin for maintaining ion homeostasis around cochlear HCs to ensure their survival. The Tric(-/-) mouse provides a new model for understanding the distinct roles of tricellulin in different epithelial systems as well as in the pathogenesis of DFNB49.
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