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The deposition of pathologic misfolded proteins in neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia and amyotrophic lateral sclerosis is hypothesized to burden protein homeostatic (proteostatic) machinery, potentially leading to insufficient capac...
ORGANISM(S): Mus musculus (Mouse) 
2018-08-29 | PXD010828 | Pride
To understand how mutations in Matrin 3 (MATR3) cause amyotrophic lateral sclerosis (ALS) and distal myopathy, we used transcriptome and interactome analysis. We found over-expression of wild-type (WT) or F115C mutant MATR3 had little impact on gene expression in neuroglia cells. We identified ~123 ...
ORGANISM(S): Homo sapiens (Human) 
2018-08-03 | PXD008896 | Pride
Heat-shock is an acute insult to the mammalian proteome. The sudden elevation in temperature has far-reaching effects on protein metabolism, leads to a rapid inhibition of most protein synthesis, and the induction of protein chaperones. Using heat-shock in cells of neuronal (SH-SY5Y) and glial (CCF-...
ORGANISM(S): Homo sapiens (Human) 
2016-04-11 | PXD003914 | Pride
A hallmark pathology of Alzheimer’s disease (AD) is the formation of amyloid ß (Aß) deposits that exhibit diverse localization and morphologies, ranging from diffuse to cored-neuritic deposits in brain parenchyma, with cerebral vascular deposition in leptomeningeal and parenchymal compartments. Most...
ORGANISM(S): Mus musculus (Mouse) 
2020-04-15 | PXD017916 | Pride
Heat-shock is an acute insult to the mammalian proteome. The sudden elevation in temperature has far-reaching effects on protein metabolism, leads to a rapid inhibition of most protein synthesis, and the induction of protein chaperones. Using heat-shock in human HEK293 cells, in conjunction with det...
ORGANISM(S): Homo sapiens (Human) 
2016-04-11 | PXD003888 | Pride
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