ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026Review
- The Role of Thyroid Hormone Signaling in the Development and Pathophysiology of Hearing: From Molecular Mechanisms to Clinical Applications.International journal of molecular sciences · 2026Review
- Engineered Inner Ear Drug Delivery Systems for Hearing Loss Treatment.Research (Washington, D.C.) · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
Gap junction Beta 2 Protein (GJB2, Connexin26, Cx26), the primary genetic cause of hereditary hearing loss (25%-50% of cases), has been exclusively regarded as forming an intercellular channel that mediates rapid communication. Here, we redefine its biological role by discovering its nuclear localization and direct transcriptional regulatory function in cochlear structure development. We demonstrate that Cx26 could aggregate in the nucleus of cochlear support cell and cell lines. Cx26 can bind to the promoter transcription start point of genomic DNA and directly regulate gene transcription, thus controlling the structural development of the tunnel of Corti during cochlear development. Further, we provide strategies based on mechanisms to promote the TC development and hearing rescue in Cx26 deficient cochlea, which has important implications for the discovery and development of treatment strategies for hearing loss caused by Cx26 deficiency.
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Registered trials
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