The LRRK2 kinase substrates Rab8a and Rab10 contribute complementary but distinct disease-relevant phenotypes in human neurons
Adamantios Mamais, Anwesha Sanyal, Austin Fajfer, Catherine G. Zykoski, Michael Guldin, Alexis Riley-DiPaolo, Nitya Subrahmanian, Whitney S. Gibbs, Steve Lin, Matthew J. LaVoie
This study shows that Rab8a and Rab10 deficiencies cause distinct lysosomal and Golgi defects in human neurons, with opposing effects on lysosomal pH and proteostasis of α-synuclein and tau.
Stem Cell Reports · Feb 1, 2024Peer-reviewedNeuroscience