ArticleHistochemistry and cell biology2014
ERADication of EDEM1 occurs by selective autophagy and requires deglycosylation by cytoplasmic peptide N-glycanase.
Article in Histochemistry and cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Cytosolic Peptide: N-Glycanase (NGLY1)-from Basic Biology to Genetic Disorder, NGLY1 Deficiency.Advances in experimental medicine and biology · 2026Review
- NGLY1 as an Emerging Critical Modulator for Neurodevelopment and Pathogenesis in the Brain.International journal of molecular sciences · 2025Review
- Turnover of EDEM1, an ERAD-enhancing factor, is mediated by multiple degradation routes.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Impact of interorganelle coordination between the conventional early secretory pathway and autophagy in cellular homeostasis and stress response.Frontiers in cell and developmental biology · 2023Review
- NGLY1 Deficiency, a Congenital Disorder of Deglycosylation: From Disease Gene Function to Pathophysiology.Cells · 2022Review
- Spermidine and Rapamycin Reveal Distinct Autophagy Flux Response and Cargo Receptor Clearance Profile.Cells · 2021Article
- Huntington's Disease Pathogenesis Is Modified In Vivo by Alfy/Wdfy3 and Selective Macroautophagy.Neuron · 2020Article
- Selective autophagy of cytosolic protein aggregates involves ribosome-free rough endoplasmic reticulum.Histochemistry and cell biology · 2020Article
- Crosstalk Between Mammalian Autophagy and the Ubiquitin-Proteasome System.Frontiers in cell and developmental biology · 2018Review
- Quality control of glycoprotein folding and ERAD: the role of N-glycan handling, EDEM1 and OS-9.Histochemistry and cell biology · 2017Review
- Varicella-Zoster Virus Infectious Cycle: ER Stress, Autophagic Flux, and Amphisome-Mediated Trafficking.Pathogens (Basel, Switzerland) · 2016Review
- Human genome-wide RNAi screen reveals host factors required for enterovirus 71 replication.Nature communications · 2016Article
- Identification of the nuclear localisation signal of O-GlcNAc transferase and its nuclear import regulation.Scientific reports · 2016Article
- The cytoplasmic peptide:N-glycanase (NGLY1) - Structure, expression and cellular functions.Gene · 2016Review
- The Role of Lectin-Carbohydrate Interactions in the Regulation of ER-Associated Protein Degradation.Molecules (Basel, Switzerland) · 2015Review
- The Histochemistry and Cell Biology pandect: the year 2014 in review.Histochemistry and cell biology · 2015Review
- Endo-β-N-acetylglucosaminidase forms N-GlcNAc protein aggregates during ER-associated degradation in Ngly1-defective cells.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ER degradation-enhancing α-mannosidase-like 1 protein (EDEM1) is involved in the routing of misfolded glycoproteins for degradation in the cytoplasm. Previously, we reported that EDEM1 leaves the endoplasmic reticulum via non-COPII vesicles (Zuber et al. in Proc Natl Acad Sci USA 104:4407-4412, 2007) and becomes degraded by basal autophagy (Le Fourn et al. in Cell Mol Life Sci 66:1434-1445, 2009). However, it is unknown which type of autophagy is involved. Likewise, how EDEM1 is targeted to autophagosomes remains elusive. We now show that EDEM1 is degraded by selective autophagy. It colocalizes with the selective autophagy cargo receptors p62/SQSTM1, neighbor of BRCA1 gene 1 (NBR1) and autophagy-linked FYVE (Alfy) protein, and becomes engulfed by autophagic isolation membranes. The interaction with p62/SQSTM1 and NBR1 is required for routing of EDEM1 to autophagosomes since it can be blocked by short inhibitory RNA knockdown of the cargo receptors. Furthermore, p62/SQSTM1 interacts only with deglycosylated EDEM1 that is also ubiquitinated. The deglycosylation of EDEM1 occurs by the cytosolic peptide N-glycanase and is a prerequisite for interaction and aggregate formation with p62/SQSTM1 as demonstrated by the effect of peptide N-glycanase inhibitors on the formation of protein aggregates. Conversely, aggregation of p62/SQSTM1 and EDEM1 occurs independent of cytoplasmic histone deacetylase. These data provide novel insight into the mechanism of autophagic degradation of the ER-associated protein degradation (ERAD) component EDEM1 and disclose hitherto unknown parallels with the clearance of cytoplasmic aggregates of misfolded proteins by selective autophagy.
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