Enrica Barchi

ALS amyotrophic lateral sclerosis ARE antioxidant response element cAMP cyclic adenosine monophosphate cGMP cyclic guanosine monophosphate CRBN cereblon DUB deubiquitinating enzyme ER endoplasmic reticulum ERAD endoplasmic reticulum–associated degradation FTD frontotemporal dementia HD Huntington's disease IGF-1 insulin-like growth factor 1 MbTAC Midnolin-based targeting chimeras MSP multisystem proteinopathy mTOR mechanistic target of rapamycin NFE2L1 nuclear factor erythroid 2-related...

Abstract The accumulation of protein aggregates has been causatively linked to the pathogenesis of neurodegenerative diseases. Here, we conduct a genome-wide CRISPR-Cas9 screen to identify cellular factors that regulate the degradation of an aggregation-prone reporter. Genes encoding proteins involved in mitochondrial homeostasis, including the translation factor eIF5A, are enriched among suppressors of the degradation of the reporter.

Abstract The accumulation of protein aggregates has been causatively linked to the pathogenesis of neurodegenerative diseases. In this study, we have conducted a genome-wide CRISPR-Cas9 screen to identify cellular factors that stimulate the degradation of an aggregation-prone reporter protein.