ArticleHearing research2016
A comprehensive catalogue of the coding and non-coding transcripts of the human inner ear.
Article in Hearing research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 3 of them syntheses that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 3 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- Utilizing Single Cell RNA-Sequencing to Implicate Cell Types and Therapeutic Targets for SSNHL in the Adult Cochlea.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2021Pooled it
- Systematic Review of Sequencing Studies and Gene Expression Profiling in Familial Meniere Disease.Genes · 2020Pooled it
- Genome-wide association meta-analysis identifies five novel loci for age-related hearing impairment.Scientific reports · 2019Pooled it
- Hearing impairment locus heterogeneity and identification of PLS1 as a new autosomal dominant gene in Hungarian Roma.European journal of human genetics : EJHG · 2019Trial
- Novel candidate genes for vestibular function identified through GWAS in the hybrid mouse diversity panel.BMC genomics · 2026Article
- Revealing heterogeneity and damage response in the adult human utricle.Nature communications · 2025Article
- Article
- Exome variant prioritization in a large cohort of hearing-impaired individuals indicates IKZF2 to be associated with non-syndromic hearing loss and guides future research of unsolved cases.Human genetics · 2024Article
- Molecular Specializations Underlying Phenotypic Differences in Inner Ear Hair Cells of Zebrafish and Mice.bioRxiv : the preprint server for biology · 2024Article
- Altered Fhod3 expression involved in progressive high-frequency hearing loss via dysregulation of actin polymerization stoichiometry in the cuticular plate.PLoS genetics · 2024Article
- A cell type-specific approach to elucidate the role of miR-96 in inner ear hair cells.Frontiers in audiology and otology · 2024Article
- Molecular specializations underlying phenotypic differences in inner ear hair cells of zebrafish and mice.Frontiers in neurology · 2024Article
- Advanced Omics Techniques for Understanding Cochlear Genome, Epigenome, and Transcriptome in Health and Disease.Biomolecules · 2023Review
- Rare-variant association analysis reveals known and new age-related hearing loss genes.European journal of human genetics : EJHG · 2023Article
- Syntaxin 4 is essential for hearing in human and zebrafish.Human molecular genetics · 2023Article
- The long and short: Non-coding RNAs in the mammalian inner ear.Hearing research · 2023Review
- The genetic contribution of the X chromosome in age-related hearing loss.Frontiers in genetics · 2023Article
- The Genomics of Auditory Function and Disease.Annual review of genomics and human genetics · 2022Review
- Identification of autosomal recessive nonsyndromic hearing impairment genes through the study of consanguineous and non-consanguineous families: past, present, and future.Human genetics · 2022Review
- The noncoding genome and hearing loss.Human genetics · 2022Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
The mammalian inner ear consists of the cochlea and the vestibular labyrinth (utricle, saccule, and semicircular canals), which participate in both hearing and balance. Proper development and life-long function of these structures involves a highly complex coordinated system of spatial and temporal gene expression. The characterization of the inner ear transcriptome is likely important for the functional study of auditory and vestibular components, yet, primarily due to tissue unavailability, detailed expression catalogues of the human inner ear remain largely incomplete. We report here, for the first time, comprehensive transcriptome characterization of the adult human cochlea, ampulla, saccule and utricle of the vestibule obtained from patients without hearing abnormalities. Using RNA-Seq, we measured the expression of >50,000 predicted genes corresponding to approximately 200,000 transcripts, in the adult inner ear and compared it to 32 other human tissues. First, we identified genes preferentially expressed in the inner ear, and unique either to the vestibule or cochlea. Next, we examined expression levels of specific groups of potentially interesting RNAs, such as genes implicated in hearing loss, long non-coding RNAs, pseudogenes and transcripts subject to nonsense mediated decay (NMD). We uncover the spatial specificity of expression of these RNAs in the hearing/balance system, and reveal evidence of tissue specific NMD. Lastly, we investigated the non-syndromic deafness loci to which no gene has been mapped, and narrow the list of potential candidates for each locus. These data represent the first high-resolution transcriptome catalogue of the adult human inner ear. A comprehensive identification of coding and non-coding RNAs in the inner ear will enable pathways of auditory and vestibular function to be further defined in the study of hearing and balance. Expression data are freely accessible at https://www.tgen.org/home/research/research-divisions/neurogenomics/supplementary-data/inner-ear-transcriptome.aspx.
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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.