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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: PINK1/PARKIN signalling in neurodegeneration and neuroinflammation

Fig. 2

The canonical PINK1/PARKIN pathway. a and b In healthy mitochondria, PINK1 is constitutively imported via translocase of the outer membrane (TOM)/translocase of the inner membrane (TIM)23 complexes to the inner mitochondrial membrane (IMM), cleaved by two proteases (mitochondrial processing peptidase (MPP) and presenilin-associated rhomboid-like (PARL)) and retro-translocated to the cytosol. Cleaved PINK1 is then degraded by the ubiquitin/proteasome system. While Parkin remains inactive in the cytosol. (a and c) PINK1 is also present at the mitochondria-endoplasmic reticulum (ER) interface, where it interacts with the endoplasmic-reticulum-associated protein degradation (ERAD) machinery. At the ER, PINK1 degradation by the proteasome is controlled by the ERAD E3 ubiquitin ligases HRD1 and gp78 and by the ERAD-associated proteins VCP, UFD1, andUFD2A

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