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Gap junction beta-2 protein (connexin 26, Cx26) is an integral membrane protein encoded by the *GJB2* gene. It forms gap junctions—specialized intercellular channels—that allow the direct exchange of ions, metabolites, and signaling molecules between adjacent cells, thus supporting tissue homeostasis and coordinated cellular function. Cx26 is abundantly expressed in the cochlea of the inner ear where it is essential for potassium ion transport critical in auditory transduction, as well as in the epidermis where it regulates growth and differentiation. Mutations in *GJB2* are the most frequent genetic cause of congenital, non-syndromic hearing loss worldwide. Additionally, abnormal expression of Cx26 has been linked with tumorigenesis, serving as both a prognostic marker (where high expression correlates with tumor progression and chemoresistance in several cancers) and a potential therapeutic target. Cx26 mutations are also involved in skin diseases and syndromic disorders combining hearing loss and dermatological symptoms.
Inhibition or modulation of gap junction intercellular communication, especially by altering the assembly, trafficking, or function of connexin 26 channels
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