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Article

VPS35 dysfunction impairs lysosomal degradation of α-synuclein and exacerbates neurotoxicity in a Drosophila model of Parkinson's disease.

Neurobiology of disease - 1 Nov 2014

Miura Emiko, Hasegawa Takafumi, Konno Masatoshi, Suzuki Mari, Sugeno Naoto, Fujikake Nobuhiro, Geisler Sven, Tabuchi Mitsuaki, Oshima Ryuji, Kikuchi Akio, Baba Toru, Wada Keiji, Nagai Yoshitaka, Takeda Atsushi, Aoki Masashi

Abstract excerpt

Mutations in vacuolar protein sorting 35 (VPS35) have been linked to familial Parkinson's disease (PD). VPS35, a component of the retromer, mediates the retrograde transport of cargo from the endosome to the trans-Golgi network. Here we showed that retromer depletion increases the lysosomal turnover of the mannose 6-phosphate receptor, thereby affecting the trafficking of cathepsin D (CTSD), a lysosome protease...

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Source

Identifiers

PMID: 25107340
DOI: 10.1016/j.nbd.2014.07.014

Genes

VPS35
CTSD

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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VPS35 dysfunction impairs lysosomal degradation of α-synuclein and exacerbates neurotoxicity in a Drosophila model of Parkinson's disease.PMID 25107340Read ↗

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