{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["70(15)"],"submitter":["Alonzi DS"],"pubmed_abstract":["Endoplasmic reticulum-associated degradation (ERAD) is a key cellular process whereby misfolded proteins are removed from the endoplasmic reticulum (ER) for subsequent degradation by the ubiquitin/proteasome system. In the present work, analysis of the released, free oligosaccharides (FOS) derived from all glycoproteins undergoing ERAD, has allowed a global estimation of the mechanisms of this pathway rather than following model proteins through degradative routes. Examining the FOS produced in endomannosidase-compromised cells following α-glucosidase inhibition has revealed a mechanism for clearing Golgi-retrieved glycoproteins that have failed to enter the ER quality control cycle. The Glc3Man7GlcNAc2 FOS species has been shown to be produced in the ER lumen by a mechanism involving a pe"],"journal":["Cellular and molecular life sciences : CMLS"],"pagination":["2799-814"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11113499"],"repository":["biostudies-literature"],"pubmed_title":["Glycoprotein misfolding in the endoplasmic reticulum: identification of released oligosaccharides reveals a second ER-associated degradation pathway for Golgi-retrieved proteins."],"pmcid":["PMC11113499"],"pubmed_authors":["Hakki Z","Williams SJ","Butters TD","Alonzi DS","Kukushkin NV","Allman SA","Pierce L","Dwek RA"],"additional_accession":[]},"is_claimable":false,"name":"Glycoprotein misfolding in the endoplasmic reticulum: identification of released oligosaccharides reveals a second ER-associated degradation pathway for Golgi-retrieved proteins.","description":"Endoplasmic reticulum-associated degradation (ERAD) is a key cellular process whereby misfolded proteins are removed from the endoplasmic reticulum (ER) for subsequent degradation by the ubiquitin/proteasome system. In the present work, analysis of the released, free oligosaccharides (FOS) derived from all glycoproteins undergoing ERAD, has allowed a global estimation of the mechanisms of this pathway rather than following model proteins through degradative routes. Examining the FOS produced in endomannosidase-compromised cells following α-glucosidase inhibition has revealed a mechanism for clearing Golgi-retrieved glycoproteins that have failed to enter the ER quality control cycle. The Glc3Man7GlcNAc2 FOS species has been shown to be produced in the ER lumen by a mechanism involving a pe","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Aug","modification":"2026-06-02T02:21:18.597Z","creation":"2026-04-13T03:12:24.882Z"},"accession":"S-EPMC11113499","cross_references":{"pubmed":["23503623"],"doi":["10.1007/s00018-013-1304-6"]}}