ER-misfolded proteins become sequestered with mitochondria and impair mitochondrial function

Sanchón et al find that misfolded proteins formed in the ER can become associated with mitochondria, both in mammalian cells and in yeast, resulting in impaired mitochondrial function. They further discover that components of ERMES-mediated ER-mitochondria contacts are needed for this mechanism, whi...

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Autores principales: Adrián Cortés Sanchón, Harshitha Santhosh Kumar, Matilde Mantovani, Ivan Osinnii, José María Mateos, Andres Kaech, Dimitri Shcherbakov, Rashid Akbergenov, Erik C. Böttger
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/bf08851619654161a435709327ef2900
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Sumario:Sanchón et al find that misfolded proteins formed in the ER can become associated with mitochondria, both in mammalian cells and in yeast, resulting in impaired mitochondrial function. They further discover that components of ERMES-mediated ER-mitochondria contacts are needed for this mechanism, which they name ERAMS, for ER-associated mitochondrial sequestration.