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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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Bibliografski detalji
Izdano u:Biochem Biophys Rep
Glavni autori: Urushima, Yuto, Haraguchi, Misa, Yano, Masato
Format: Artigo
Jezik:Inglês
Izdano: Elsevier 2020
Teme:
Online pristup:https://ncbi.nlm.nih.gov/pmc/articles/PMC7725676/
https://ncbi.nlm.nih.gov/pubmed/33319071
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.bbrep.2020.100870
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