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Ubiquitin Project

The elucidation of molecular mechanisms underlying ubiquitin signaling and the related disorders Project

Project Leader Yasuko Ono

Project Leader
Noriyuki Matsuda

Backgrounds

In cells, ubiquitin governs the life and death of various proteins and cell organelles as a factor that determines their fate. In recent years, it has been suggested that ubiquitin abnormalities are closely related to various diseases including Parkinson’s.

This project, along with elucidating ubiquitin’s role in the body, which until now has been shrouded in mystery, seeks to reveal its association with neurodegenerative diseases such as Parkinson’s.

Objectives

  • To pay attention to ubiquitin when examining the pathogenesis of neurodegenerative diseases such as Parkinson’s
  • To produce an animal disease model through modification of the in vivo ubiquitin environment
  • To help maintain people’s health by clarifying the function that ubiquitin plays in various roles in the body

Members

Project Leader Noriyuki Matsuda

  • Yukiko Yoshida
  • Koji Yamano
  • Fumika Koyano
  • Reika Yamagishi
  • Waka Kojima

Selected Publications

  • Yamano K, Wang C, Sarraf S, Münch C, Kikuchi R, Noda N, Hizukuri Y, Kanemaki M, Harper W, Tanaka K, Matsuda N, and Youle R. (2018) “Endosomal Rab cycles regulate Parkin-mediated mitophagy.” eLife 7: e31326
  • Okatsu K, Koyano F, Kimura M, Kosako H, Saeki Y, Tanaka K, and Matsuda N. (2015) “Phosphorylated ubiquitin chain is the genuine Parkin receptor.” J. Cell Biology 209:111-128
  • Koyano F, Okatsu K, Kosako H, Tamura Y, Go E, Kimura M, Kimura Y, Tsuchiya H, Yoshihara H, Hirokawa T, Endo T, Fon E-A, Trempe J-F, Saeki Y, Tanaka K, and Matsuda N. (2014) “Ubiquitin is phosphorylated by PINK1 to activate Parkin.” Nature 510, 162-166.
  • Okatsu K, Oka T, Iguchi M, Imamura K, Kosako H, Tani N, Kimura M, Go E, Koyano F, Funayama M, Shiba-Fukushima K, Sato S, Shimizu H, Fukunaga Y, Taniguchi H, Komatsu M, Hattori N, Mihara K, Tanaka K, and Matsuda N. (2012) “PINK1 autophosphorylation upon membrane potential dissipation is essential for Parkin recruitment to damaged mitochondria.” Nature Commun. 3 : e1016 (10 pages).
  • Matsuda N, Sato S, Shiba K, Okatsu K, Saisho K, Gautier C, Sou Y-S, Saiki S, Kawajiri S, Sato F, Kimura M, Komatsu M, Hattori N, and Tanaka K. (2010) “PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy.” J. Cell Biology 189: 211-221