ArticleScientific reports2017
Indispensable role of Mdm2/p53 interaction during the embryonic and postnatal inner ear development.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- The ubiquitin-proteasome system and proteostasis in the cochlea and sensorineural hearing disorders.Molecular biomedicine · 2026Review
- Ubiquitination of MEIS1 by MDM2 serves as a switch for p53 stabilization and DNA damage response activation.Cell death and differentiation · 2026Article
- MicroRNAs as potential biomarkers for monitoring of acquired sensorineural hearing loss.Pediatric discovery · 2024Review
- GRAIL gene knockout mice protect against aging-related and noise-induced hearing loss.Journal of the Chinese Medical Association : JCMA · 2023Article
- Ubiquitin ligases: guardians of mammalian development.Nature reviews. Molecular cell biology · 2022Review
- Targeting MDM2 for novel molecular therapy: Beyond oncology.Medicinal research reviews · 2020Review
- E3 ubiquitin ligase MDM2 acts through p53 to control respiratory progenitor cell number and lung size.Development (Cambridge, England) · 2019Article
- The Stress Response in the Non-sensory Cells of the Cochlea Under Pathological Conditions-Possible Role in Mediating Noise Vulnerability.Journal of the Association for Research in Otolaryngology : JARO · 2018Article
- Characterization of Lgr5+ Progenitor Cell Transcriptomes after Neomycin Injury in the Neonatal Mouse Cochlea.Frontiers in molecular neuroscience · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 is a key component of a signaling network that protects cells against various stresses. As excess p53 is detrimental to cells, its levels are tightly controlled by several mechanisms. The E3 ubiquitin ligase Mdm2 is a major negative regulator of p53. The significance of balanced p53 levels in normal tissues, at different stages of lifetime, is poorly understood. We have studied in vivo how the disruption of Mdm2/p53 interaction affects the early-embryonic otic progenitor cells and their descendants, the auditory supporting cells and hair cells. We found that p53 accumulation, as a consequence of Mdm2 abrogation, is lethal to both proliferative progenitors and non-proliferating, differentiating cells. The sensitivity of postmitotic supporting cells to excess p53 decreases along maturation, suggesting that maturation-related mechanisms limit p53's transcriptional activity towards pro-apoptotic factors. We have also investigated in vitro whether p53 restricts supporting cell's regenerative capacity. Unlike in several other regenerative cellular models, p53 inactivation did not alter supporting cell's proliferative quiescence nor transdifferentiation capacity. Altogether, the postmitotic status of developing hair cells and supporting cells does not confer protection against the detrimental effects of p53 upregulation. These findings might be linked to auditory disturbances observed in developmental syndromes with inappropriate p53 upregulation.
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