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Amyloid-like aggregating proteins cause lysosomal defects in neurons via gain-of-function toxicity

ABSTRACT: Here, we combine cryo-electron tomography, proteomics and cell biology studies to investigate the effects of protein aggregates in primary neurons. We use artificial amyloid-like β-sheet proteins (β proteins) to focus on the gain-of-function aspect of aggregation. These proteins form fibrillar aggregates and cause neurotoxicity. We show that late stages of autophagy are impaired by the aggregates, resulting in lysosomal alterations reminiscent of lysosomal storage disorders.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Primary Cell, Neural Tissue

DISEASE(S): Neurodegenerative Disease

SUBMITTER: Daniel Hornburg

LAB HEAD: Daniel Hornburg

PROVIDER: PXD029689 | Pride | 2021-12-20

REPOSITORIES: Pride

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			Action	DRS
	20150213_QEp4_DaHo_SA_neurons_B17_1.raw	Raw
	20150213_QEp4_DaHo_SA_neurons_B17_2.raw	Raw
	20150213_QEp4_DaHo_SA_neurons_B17_3.raw	Raw
	20150213_QEp4_DaHo_SA_neurons_B17_4.raw	Raw
	20150213_QEp4_DaHo_SA_neurons_B23_1.raw	Raw

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