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Autophagic Punctum

The retroviral restriction factor TRIM5/TRIM5α regulates mitochondrial quality control

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Pages 372-373 | Received 25 May 2022, Accepted 27 May 2022, Published online: 05 Jun 2022

Figures & data

Figure 1. Following mitochondrial damage, TRIM5 localizes to ER-mitochondrial contact sites where it recruits the autophagy initiation machinery, including ULK1 complex proteins, to proteins tagging damaged mitochondria (eat-me tags). In the absence of TRIM5, the recruitment of autophagy proteins to damaged mitochondria is abrogated, mitophagy is impaired, and cells show elevated inflammatory responses to mitochondrial damage. Abbreviations: ER, endoplasmic reticulum; PG, phagophore. Figure was created using BioRender.

Figure 1. Following mitochondrial damage, TRIM5 localizes to ER-mitochondrial contact sites where it recruits the autophagy initiation machinery, including ULK1 complex proteins, to proteins tagging damaged mitochondria (eat-me tags). In the absence of TRIM5, the recruitment of autophagy proteins to damaged mitochondria is abrogated, mitophagy is impaired, and cells show elevated inflammatory responses to mitochondrial damage. Abbreviations: ER, endoplasmic reticulum; PG, phagophore. Figure was created using BioRender.

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