Mitochondrial E3 ubiquitin ligase parkin: Relationships with other causal proteins in familial parkinson’s disease and its substrate-involved mouse experimental models

Satoru Torii, Shuya Kasai, Tatsushi Yoshida, Ken Ichi Yasumoto, Shigeomi Shimizu

研究成果: Review article査読

4 被引用数 (Scopus)

抄録

Parkinson’s disease (PD) is a common neurodegenerative disorder. Recent identification of genes linked to familial forms of PD has revealed that post-translational modifications, such as phosphorylation and ubiquitination of proteins, are key factors in disease pathogenesis. In PD, E3 ubiquitin ligase Parkin and the serine/threonine-protein kinase PTEN-induced kinase 1 (PINK1) mediate the mitophagy pathway for mitochondrial quality control via phosphorylation and ubiquitination of their substrates. In this review, we first focus on well-characterized PINK1 phosphorylation motifs. Second, we describe our findings concerning relationships between Parkin and HtrA2/Omi, a protein involved in familial PD. Third, we describe our findings regarding inhibitory PAS (Per/Arnt/Sim) domain protein (IPAS), a member of PINK1 and Parkin substrates, involved in neurodegeneration during PD. IPAS is a dual-function protein involved in transcriptional repression of hypoxic responses and the pro-apoptotic activities.

本文言語English
論文番号1202
ジャーナルInternational journal of molecular sciences
21
4
DOI
出版ステータスPublished - 2020 2月 2

ASJC Scopus subject areas

  • 触媒
  • 分子生物学
  • 分光学
  • コンピュータ サイエンスの応用
  • 物理化学および理論化学
  • 有機化学
  • 無機化学

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