ArticleStem cell reports2021
HIC1 Represses Atoh1 Transcription and Hair Cell Differentiation in the Cochlea.
Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Trimodal single-cell profiling of transcriptome, epigenome and 3D genome in complex tissues with scHiCAR.Nature biotechnology · 2026Article
- Inner Ear Organoids: A Hydrogel-Based Platform for Drug Screening and Deafness Modeling.Neuroscience bulletin · 2026Review
- Inner ear organoids: Recent progress and potential applications.Fundamental research · 2025Review
- Conditional Overexpression of Serpine2 Promotes Hair Cell Regeneration from Lgr5+ Progenitors in the Neonatal Mouse Cochlea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sox2 interacts with Atoh1 and Huwe1 loci to regulate Atoh1 transcription and stability during hair cell differentiation.PLoS genetics · 2025Article
- Precise genetic control of ATOH1 enhances maturation of regenerated hair cells in the mature mouse utricle.Nature communications · 2024Article
- Article
- Loss of ATOH1 in Pit Cell Drives Stemness and Progression of Gastric Adenocarcinoma by Activating AKT/mTOR Signaling through GAS1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Gene therapy: an emerging therapy for hair cells regeneration in the cochlea.Frontiers in neuroscience · 2023Review
- The regenerative capacity of neonatal tissues.Development (Cambridge, England) · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Across species, expression of the basic helix-loop-helix transcription factor ATOH1 promotes differentiation of cochlear supporting cells to sensory hair cells required for hearing. In mammals, this process is limited to development, whereas nonmammalian vertebrates can also regenerate hair cells after injury. The mechanistic basis for this difference is not fully understood. Hypermethylated in cancer 1 (HIC1) is a transcriptional repressor known to inhibit Atoh1 in the cerebellum. We therefore investigated its potential role in cochlear hair cell differentiation. We find that Hic1 is expressed throughout the postnatal murine cochlear sensory epithelium. In cochlear organoids, Hic1 knockdown induces Atoh1 expression and promotes hair cell differentiation, while Hic1 overexpression hinders differentiation. Wild-type HIC1, but not the DNA-binding mutant C521S, suppresses activity of the Atoh1 autoregulatory enhancer and blocks its responsiveness to β-catenin activation. Our findings reveal the importance of HIC1 repression of Atoh1 in the cochlea, which may be targeted to promote hair cell regeneration.
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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.