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experiments demonstrated that ER stress significantly reduced Cx26 protein levels in cochlear explants. Mechanistically, we observed enhanced expression of ubiquitination-related proteins Nedd4 and Eps15 with evident colocalization with Cx26 in an ER stress mouse model. In summary, our findings demonstrate that Cx26 ubiquitination mediated by cochlear ER stress is the main cause of Cx26 degradation in the cochlea of aged mice.
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Bai et al. (2025) studied this question.
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