ArticleThe Journal of biological chemistry2011
Mannose trimming is required for delivery of a glycoprotein from EDEM1 to XTP3-B and to late endoplasmic reticulum-associated degradation steps.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- Article
- HCMV US2 co-opts TRC8 to degrade the endoplasmic reticulum-resident protein LMAN2L.The Journal of general virology · 2024Article
- OrthoID: profiling dynamic proteomes through time and space using mutually orthogonal chemical tools.Nature communications · 2024Article
- AUP1 Regulates the Endoplasmic Reticulum-Associated Degradation and Polyubiquitination of NKCC2.Cells · 2024Article
- 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
- Differential Effects of STCH and Stress-Inducible Hsp70 on the Stability and Maturation of NKCC2.International journal of molecular sciences · 2021Article
- Review
- Proteostasis Failure in Neurodegenerative Diseases: Focus on Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- Sugar-Recognizing Ubiquitin Ligases: Action Mechanisms and Physiology.Frontiers in physiology · 2019Review
- Abnormal expression of ER quality control and ER associated degradation proteins in the dorsolateral prefrontal cortex in schizophrenia.Schizophrenia research · 2018Article
- Mannosidase activity of EDEM1 and EDEM2 depends on an unfolded state of their glycoprotein substrates.Communications biology · 2018Article
- The Pathogen-Occupied Vacuoles of Anaplasma phagocytophilum and Anaplasma marginale Interact with the Endoplasmic Reticulum.Frontiers in cellular and infection microbiology · 2016Article
- 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
- Hydrophobicity of protein determinants influences the recognition of substrates by EDEM1 and EDEM2 in human cells.BMC cell biology · 2015Article
- Reglucosylation by UDP-glucose:glycoprotein glucosyltransferase 1 delays glycoprotein secretion but not degradation.Molecular biology of the cell · 2015Article
- Mammalian ER mannosidase I resides in quality control vesicles, where it encounters its glycoprotein substrates.Molecular biology of the cell · 2015Article
- Endoplasmic reticulum degradation-enhancing α-mannosidase-like protein 1 targets misfolded HLA-B27 dimers for endoplasmic reticulum-associated degradation.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Recent technical developments in the study of ER-associated degradation.Current opinion in cell biology · 2014Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the trimming of α1,2-mannose residues from precursor N-linked oligosaccharides is an essential step in the delivery of misfolded glycoproteins to endoplasmic reticulum (ER)-associated degradation (ERAD), the exact role of this trimming is unclear. EDEM1 was initially suggested to bind N-glycans after mannose trimming, a role presently ascribed to the lectins OS9 and XTP3-B, because of their in vitro affinities for trimmed oligosaccharides. We have shown before that ER mannosidase I (ERManI) is required for the trimming and concentrates together with the ERAD substrate and ERAD machinery in the pericentriolar ER-derived quality control compartment (ERQC). Inhibition of mannose trimming prevents substrate accumulation in the ERQC. Here, we show that the mannosidase inhibitor kifunensine or ERManI knockdown do not affect binding of an ERAD substrate glycoprotein to EDEM1. In contrast, substrate association with XTP3-B and with the E3 ubiquitin ligases HRD1 and SCF(Fbs2) was inhibited. Consistently, whereas the ERAD substrate partially colocalized upon proteasomal inhibition with EDEM1, HRD1, and Fbs2 at the ERQC, colocalization was repressed by mannosidase inhibition in the case of the E3 ligases but not for EDEM1. Interestingly, association and colocalization of the substrate with Derlin-1 was independent of mannose trimming. The HRD1 adaptor protein SEL1L had been suggested to play a role in N-glycan-dependent substrate delivery to OS9 and XTP3-B. However, substrate association with XTP3-B was still dependent on mannose trimming upon SEL1L knockdown. Our results suggest that mannose trimming enables delivery of a substrate glycoprotein from EDEM1 to late ERAD steps through association with XTP3-B.
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