Loss of Ezrin triggers mitochondrial dysfunction and oxidative stress, associated with neuronal cell death.

ABSTRACT: EZRIN is a key player in assembling and coordinating molecular signaling, acting as a linker between receptors in plasma membrane and the actin cytoskeleton. High EZRIN expression level has been extensively studied and often associated with metastasis and cancer progression. Recent reports independently suggested associations between Ezrin and mitochondrial alterations or apoptotic processes, the mechanism by which Ezrin modulates these events remain largely unclear. Here we report that the lack of EZRIN-mediated EGFR internalization and translocation on mitochondria is critical for mitochondrial metabolism. Ezrin-deficient (Ezrin^-/-) cells exhibit marked impairments in mitochondrial respiratory chain (MRC) activity. These cells also show significantly reduced ATP production and

SUBMITTER: Giamundo G 

PROVIDER: S-EPMC12559342 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature