{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yuan R"],"funding":["National Institute of Neurological Disorders and Stroke","NINDS NIH HHS","NIGMS NIH HHS"],"pagination":["570-596"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9851260"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(2)"],"pubmed_abstract":["Neurons and astrocytes face unique demands on their proteome to enable proper function and survival of the nervous system. Consequently, both cell types are critically dependent on robust quality control pathways such as macroautophagy (hereafter referred to as autophagy) and the ubiquitin-proteasome system (UPS). We previously reported that autophagy is differentially regulated in astrocytes and neurons in the context of metabolic stress, but less is understood in the context of proteotoxic stress induced by inhibition of the UPS. Dysfunction of the proteasome or autophagy has been linked to the progression of various neurodegenerative diseases. Therefore, in this study, we explored the connection between autophagy and the proteasome in primary astrocytes and neurons. Prior studies largel"],"journal":["Autophagy"],"pubmed_title":["Proteasomal inhibition preferentially stimulates lysosome activity relative to autophagic flux in primary astrocytes."],"pmcid":["PMC9851260"],"funding_grant_id":["R01 NS110716","R01NS110716","R00 NS082619","R00NS082619","T32 GM144290"],"pubmed_authors":["Stempel MH","Kulkarni A","Sidibe DK","Chen J","Yuan R","Hahn Y","Laxton O","Maday S"],"additional_accession":[]},"is_claimable":false,"name":"Proteasomal inhibition preferentially stimulates lysosome activity relative to autophagic flux in primary astrocytes.","description":"Neurons and astrocytes face unique demands on their proteome to enable proper function and survival of the nervous system. Consequently, both cell types are critically dependent on robust quality control pathways such as macroautophagy (hereafter referred to as autophagy) and the ubiquitin-proteasome system (UPS). We previously reported that autophagy is differentially regulated in astrocytes and neurons in the context of metabolic stress, but less is understood in the context of proteotoxic stress induced by inhibition of the UPS. Dysfunction of the proteasome or autophagy has been linked to the progression of various neurodegenerative diseases. Therefore, in this study, we explored the connection between autophagy and the proteasome in primary astrocytes and neurons. Prior studies largel","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-05-07T14:09:28.162Z","creation":"2025-04-04T07:38:02.068Z"},"accession":"S-EPMC9851260","cross_references":{"pubmed":["35722992"],"doi":["10.1080/15548627.2022.2084884"]}}