Mitochondrial import stress and PINK1-mediated mitophagy: the role of the PINK1-TOMM-TIMM23 supercomplex.
Autophagy
; 20(8): 1903-1905, 2024 Aug.
Article
em En
| MEDLINE
| ID: mdl-38597070
ABSTRACT
Mutations in the PINK1 kinase cause Parkinson disease (PD) through physiological processes that are not yet fully elucidated. PINK1 kinase accumulates selectively on damaged mitochondria, where it recruits the E3 ubiquitin ligase PRKN/Parkin to mediate mitophagy. Upon mitochondrial import failure, PINK1 accumulates in association with the translocase of outer mitochondrial membrane (TOMM). However, the molecular basis of this PINK1 accumulation on the TOMM complex remain elusive. We recently demonstrated that TIMM23 (translocase of the inner mitochondrial membrane 23) is a component of the PINK1-supercomplex formed in response to mitochondrial stress. We also uncovered that PINK1 is required for the formation of this supercomplex and highlighted the biochemical regulation and significance of this supercomplex; expanding our understanding of mitochondrial quality control and PD pathogenesis.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas Quinases
/
Mitofagia
/
Mitocôndrias
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Autophagy
Ano de publicação:
2024
Tipo de documento:
Article
País de afiliação:
Canadá