Proteomics

Dataset Information

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Proteomic analysis of human PARK2 knockout iPSC-derived neurons


ABSTRACT: Mitochondrial dysfunction plays a major role in the pathogenesis of sporadic Parkinson’s disease (PD) and familial PD caused by mutations in the PARK2 gene. The protein, parkin, is vital for mitochondrial function, but the lack of key PD phenotypes in PARK2 knockout (KO) rodent models has hindered investigations into parkin’s role in PD pathogenesis. Human isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 KO enable studies of the effect of parkin dysfunction in dopaminergic neuronal cultures.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Parkinson's Disease

SUBMITTER: Pia Jensen  

LAB HEAD: Martin Røssel Larsen

PROVIDER: PXD007871 | Pride | 2019-09-03

REPOSITORIES: Pride

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Publications

Perturbations in RhoA signalling cause altered migration and impaired neuritogenesis in human iPSC-derived neural cells with PARK2 mutation.

Bogetofte Helle H   Jensen Pia P   Okarmus Justyna J   Schmidt Sissel Ida SI   Agger Mikkel M   Ryding Matias M   Nørregaard Peter P   Fenger Christina C   Zeng Xianmin X   Graakjær Jesper J   Ryan Brent James BJ   Wade-Martins Richard R   Larsen Martin Røssel MR   Meyer Morten M  

Neurobiology of disease 20190821


Mutations in parkin, encoded by the PARK2 gene, causes early-onset familial Parkinson's disease (PD), but dysfunctional parkin has also been implicated in sporadic PD. By combining human isogenic induced pluripotent stem cells (iPSCs) with and without PARK2 knockout (KO) and a novel large-scale mass spectrometry based proteomics and post-translational modification (PTM)-omics approach, we have mapped changes in protein profiles and PTMs caused by parkin deficiency in neurons. Our study identifie  ...[more]

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