Depletion of TMEM65 leads to oxidative stress, apoptosis, induction of mitochondrial unfolded protein response, and upregulation of mitochondrial protein import receptor TOMM22

Mutation in the transmembrane protein 65 gene (TMEM65) results in mitochondrial dysfunction and a severe mitochondrial encephalomyopathy phenotype. However, neither the function of TMEM65 nor the cellular responses to its depletion have been fully elucidated. Hence, we knocked down TMEM65 in human c...

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Detalles Bibliográficos
Autores principales: Urushima, Yuto, Haraguchi, Misa, Yano, Masato
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7725676/
https://www.ncbi.nlm.nih.gov/pubmed/33319071
http://dx.doi.org/10.1016/j.bbrep.2020.100870

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