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. 2022 Jun 9;19(2):401–414. doi: 10.1080/15548627.2022.2084862

Figure 2.

Figure 2.

PRKN-dependent mitophagy. PINK1 is constitutively processed by mitochondrial proteases, PMP and PARL, resulting in its proteasomal degradation in normal condition (a); In damaged mitochondria, PINK1 accumulates at OMM bound to the TOMM complex where it is activated through auto-phosphorylation. Activated PINK1 subsequently phosphorylates ubiquitin, which triggers recruitment of PRKN recruitment to mitochondria and activation of its E3 ligase activity. It further ubiquitinates mitochondrial substrates and initiate autophagosome formation. PRKN acts as an enhancer of this signaling through further ubiquitination of mitochondrial proteins (b). Abbreviations: IMM: inner mitochondrial membrane; OMM: outer mitochondrial membrane; PARL: presenilin associated rhomboid like; PINK1: PTEN induced kinase 1; PMP: peptidase, mitochondrial processing; PRKN: parkin RBR E3 ubiquitin protein ligase; SQSTM1/p62: sequestosome 1; TIMM: translocase of inner mitochondrial membrane; TOMM: translocase of outer mitochondrial membrane.