Understanding PINK1/Parkin mitophagy :
from autophagosome formation to lysosomal degradation.

− この都医学研セミナーは終了しました。 −

演者 Dr. Michael Lazarou;
Department of Biochemistry and Molecular Biology Biomedicine Discovery Institute,Monash University, Australia
会場 東京都医学総合研究所 BC会議室
日時 平成29年6月9日(金)16:00~
世話人 松田 憲之 (生体分子先端研究分野 ユビキチンプロジェクトリーダー)
参加自由 詳細は下記問合せ先まで
お問い合わせ 研究推進課 普及広報係
電話 03-5316-3109


Functional mitochondria are critically important for the maintenance of cellular integrity and survival. Two gene products mutated in familial Parkinsonism, PINK1 and Parkin, function together to maintain mitochondrial health by identifying damaged mitochondria and degrading them through a selective form of autophagy termed mitophagy. PINK1 is a kinase that accumulates on the surface of damaged mitochondria where it simultaneously recruits and activates the ubiquitin ligase Parkin. PINK1/Parkin mediated ubiquitination of mitochondrial substrates forms the basis of multiple signaling events that result in engulfment of damaged mitochondria within autophagosomes, and degradation by lysosomes. I will discuss how ubiquitination promotes selective recognition of mitochondria by the autophagy machinery during PINK1/Parkin mitophagy, and the downstream steps required for autophagosome formation and maturation. Specifically, the role of ubiquitin binding autophagy receptors and Atg8 family LC3/GABARAP proteins will be explored.


Lazarou 博士は新学術領域研究「オートファジー」国際活動支援事業の一環と して当研究所を訪問されます。
(新学術領域側世話人: 東京大学 水島昇教授、福 島県立医科大学 和栗聡教授)