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Parkinson’s VPS35[D620N] retromer lysosomal dysfunction induces LRRK2 mediated lysosomal association of RILPL1 and TMEM55B

ABSTRACT: The D620N VPS35 mutation disrupts retrograde endosome to Golgi retromer Trafficking. Thus causes lysosome dysfunction, enhances LRRK2 kinase activity and leads to Parkinson’s disease. We employed a LysoTag immunoprecipitation approach to assess how this impacts lysosomes using quantitative proteomics. The VPS35[D620N] mutation alters the expression of over 350 lysosomal proteins, and induces recruitment of LRRK2 phosphorylated Rab proteins to the lysosome, as well as the phosphoRab effector protein RILPL1.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Fibroblast

DISEASE(S): Parkinson's Disease

SUBMITTER: Yuko Pui Yiu Lam

LAB HEAD: Dario R. Alessi

PROVIDER: PXD042502 | Pride | 2023-11-28

REPOSITORIES: Pride

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			Action	DRS
	20211217_YL_MEFs_Lyso_IP_D620N_S1.raw	Raw
	20211217_YL_MEFs_Lyso_IP_D620N_S2.raw	Raw
	20211217_YL_MEFs_Lyso_IP_D620N_S3.raw	Raw
	20211217_YL_MEFs_Lyso_IP_D620N_S4.raw	Raw
	20211217_YL_MEFs_Lyso_IP_D620N_S5.raw	Raw

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Dataset Information

Parkinson’s VPS35[D620N] retromer lysosomal dysfunction induces LRRK2 mediated lysosomal association of RILPL1 and TMEM55B

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