- The endoplasmic reticulum-mitochondria interface is perturbed in PARK2 knockout mice and patients with PARK2 mutations.
The endoplasmic reticulum-mitochondria interface is perturbed in PARK2 knockout mice and patients with PARK2 mutations.
Human molecular genetics (2016-05-22)
Clément A Gautier, Zoi Erpapazoglou, François Mouton-Liger, Marie Paule Muriel, Florence Cormier, Stéphanie Bigou, Sophie Duffaure, Mathilde Girard, Benjamin Foret, Angelo Iannielli, Vania Broccoli, Carine Dalle, Delphine Bohl, Patrick P Michel, Jean-Christophe Corvol, Alexis Brice, Olga Corti
PMID27206984
摘要
Mutations in PARK2, encoding the E3 ubiquitin protein ligase Parkin, are a common cause of autosomal recessive Parkinson's disease (PD). Loss of PARK2 function compromises mitochondrial quality by affecting mitochondrial biogenesis, bioenergetics, dynamics, transport and turnover. We investigated the impact of PARK2 dysfunction on the endoplasmic reticulum (ER)-mitochondria interface, which mediates calcium (Ca