ArticleCell death discovery2025
Loss of Ezrin triggers mitochondrial dysfunction and oxidative stress, associated with neuronal cell death.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- REP-1 deficiency induces aberrant mitochondrial metabolic rewiring from glycolysis to lipid oxidation in CHM disease.Cell death & disease · 2026Article
- Machine learning and bioinformatics identify and validate membrane protein biomarkers for type 2 diabetes mellitus.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
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
Identifiers
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Registered trials
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