{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Studencka-Turski M"],"funding":["Deutsche Forschungsgemeinschaft"],"pagination":["2900"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6932173"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10"],"pubmed_abstract":["Proteostasis is critical for cells to maintain the balance between protein synthesis, quality control, and degradation. This is particularly important for myeloid cells of the central nervous system as their immunological function relies on proper intracellular protein turnover by the ubiquitin-proteasome system. Accordingly, disruption of proteasome activity due to, e.g., loss-of-function mutations within genes encoding proteasome subunits, results in systemic autoinflammation. On the molecular level, pharmacological inhibition of proteasome results in endoplasmic reticulum (ER) stress-activated unfolded protein response (UPR) as well as an induction of type I interferons (IFN). Nevertheless, our understanding as to whether and to which extent UPR signaling regulates type I IFN response i"],"journal":["Frontiers in immunology"],"pubmed_title":["Molecular Insight Into the IRE1α-Mediated Type I Interferon Response Induced by Proteasome Impairment in Myeloid Cells of the Brain."],"pmcid":["PMC6932173"],"funding_grant_id":["CRC/TRR 186","SFB/TRR167"],"pubmed_authors":["Cetin G","Junker H","Ebstein F","Studencka-Turski M","Kruger E"],"additional_accession":[]},"is_claimable":false,"name":"Molecular Insight Into the IRE1α-Mediated Type I Interferon Response Induced by Proteasome Impairment in Myeloid Cells of the Brain.","description":"Proteostasis is critical for cells to maintain the balance between protein synthesis, quality control, and degradation. This is particularly important for myeloid cells of the central nervous system as their immunological function relies on proper intracellular protein turnover by the ubiquitin-proteasome system. Accordingly, disruption of proteasome activity due to, e.g., loss-of-function mutations within genes encoding proteasome subunits, results in systemic autoinflammation. On the molecular level, pharmacological inhibition of proteasome results in endoplasmic reticulum (ER) stress-activated unfolded protein response (UPR) as well as an induction of type I interferons (IFN). Nevertheless, our understanding as to whether and to which extent UPR signaling regulates type I IFN response i","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019","modification":"2025-05-29T21:04:39.379Z","creation":"2025-05-29T21:04:39.379Z"},"accession":"S-EPMC6932173","cross_references":{"pubmed":["31921161"],"doi":["10.3389/fimmu.2019.02900"]}}