ArticleMolecular biology of the cell2011
Bypass of glycan-dependent glycoprotein delivery to ERAD by up-regulated EDEM1.
Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Glycosylation as an intricate post-translational modification process takes part in glycoproteins related immunity.Cell communication and signaling : CCS · 2025Review
- EDEM1 regulates the insulin mRNA level by inhibiting the endoplasmic reticulum stress-induced IRE1/JNK/c-Jun pathway.iScience · 2023Article
- Identification of EGF Receptor and Thrombospondin-1 as Endogenous Targets of ER-Associated Degradation Enhancer EDEM1 in HeLa Cells.International journal of molecular sciences · 2023Article
- COP I and II dependent trafficking controls ER-associated degradation in mammalian cells.iScience · 2023Article
- Golgi Alpha1,2-Mannosidase IA Promotes Efficient Endoplasmic Reticulum-Associated Degradation of NKCC2.Cells · 2021Article
- EDEM1 Regulates Amyloid Precursor Protein (APP) Metabolism and Amyloid-β Production.International journal of molecular sciences · 2021Article
- TDAG51 induces renal interstitial fibrosis through modulation of TGF-β receptor 1 in chronic kidney disease.Cell death & disease · 2021Article
- EDEM3 Domains Cooperate to Perform Its Overall Cell Functioning.International journal of molecular sciences · 2021Article
- DNA methylation during human adipogenesis and the impact of fructose.Genes & nutrition · 2020Article
- Endoplasmic reticulum stress causes insulin resistance by inhibiting delivery of newly synthesized insulin receptors to the cell surface.Molecular biology of the cell · 2020Article
- The cytoplasmic tail of human mannosidase Man1b1 contributes to catalysis-independent quality control of misfolded alpha1-antitrypsin.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Review
- EDEM1 Drives Misfolded Protein Degradation via ERAD and Exploits ER-Phagy as Back-Up Mechanism When ERAD Is Impaired.International journal of molecular sciences · 2020Article
- Toxins Utilize the Endoplasmic Reticulum-Associated Protein Degradation Pathway in Their Intoxication Process.International journal of molecular sciences · 2019Review
- Modulation of ERQC and ERAD: A Broad-Spectrum Spanner in the Works of Cancer Cells?Journal of oncology · 2019Review
- Human Cytomegalovirus Tropism Modulator UL148 Interacts with SEL1L, a Cellular Factor That Governs Endoplasmic Reticulum-Associated Degradation of the Viral Envelope Glycoprotein gO.Journal of virology · 2018Article
- Mannosidase activity of EDEM1 and EDEM2 depends on an unfolded state of their glycoprotein substrates.Communications biology · 2018Article
- Unfolded Protein Response and Macroautophagy in Alzheimer's, Parkinson's and Prion Diseases.Molecules (Basel, Switzerland) · 2015Review
- The Role of Lectin-Carbohydrate Interactions in the Regulation of ER-Associated Protein Degradation.Molecules (Basel, Switzerland) · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trimming of mannose residues from the N-linked oligosaccharide precursor is a stringent requirement for glycoprotein endoplasmic reticulum (ER)-associated degradation (ERAD). In this paper, we show that, surprisingly, overexpression of ER degradation-enhancing α-mannosidase-like protein 1 (EDEM1) or its up-regulation by IRE1, as occurs in the unfolded protein response, overrides this requirement and renders unnecessary the expression of ER mannosidase I. An EDEM1 deletion mutant lacking most of the carbohydrate-recognition domain also accelerated ERAD, delivering the substrate to XTP3-B and OS9. EDEM1 overexpression also accelerated the degradation of a mutant nonglycosylated substrate. Upon proteasomal inhibition, EDEM1 concentrated together with the ERAD substrate in the pericentriolar ER-derived quality control compartment (ERQC), where ER mannosidase I and ERAD machinery components are localized, including, as we show here, OS9. We suggest that a nascent glycoprotein can normally dissociate from EDEM1 and be rescued from ERAD by reentering calnexin-refolding cycles, a condition terminated by mannose trimming. At high EDEM1 levels, glycoprotein release is prevented and glycan interactions are no longer required, canceling the otherwise mandatory ERAD timing by mannose trimming and accelerating the targeting to degradation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.