ArticleThe EMBO journal2021
N-glycan processing selects ERAD-resistant misfolded proteins for ER-to-lysosome-associated degradation.
Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Remaking an exit: dynamic regulation of ER exit sites by post-translational modifications.Trends in cell biology · 2026Review
- The ubiquitin-proteasome system and autophagy as guardians of the cellular proteome.FEBS letters · 2026Review
- Endocytome profiling uncovers cell-surface protein dynamics underlying neuronal connectivity.Neuron · 2026Article
- Gene Expression Analysis of Mitochondria-Associated Membrane (MAM)-Related Genes in ER Stress and Alzheimer's Disease.Cellular and molecular neurobiology · 2026Article
- FAM134B isoform 2/RETREG1-2 defines a calnexin-TOLLIP-coupled ER-phagy pathway that restricts Ebola virus glycoprotein and is antagonized by VP40 through macro-autophagy.bioRxiv : the preprint server for biology · 2026Article
- SDF2L1 modulates oxLDL-induced endoplasmic reticulum stress, protein aggregation, and O-mannosylation in myocardial infarction and lung cancer.Cellular and molecular life sciences : CMLS · 2026Article
- FAM134B controls collagen I dynamics in hepatic stellate cell-driven fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- The role of N-glycans and their processing in ER-to-lysosome-associated degradation of disease-causing mutant Neuroserpin.Autophagy reports · 2026Article
- Mass spectrometric profiling reveals alterations in N-Glycans and O-Glycans in Tay-Sachs disease under Autophagy-Induced conditions.Glycoconjugate journal · 2025Article
- N-glycan-dependent protein maturation and quality control in the ER.Nature reviews. Molecular cell biology · 2025Review
- Cholesterol biosynthesis as a drug-induced vulnerability in diffuse large B cell lymphoma insensitive to EZH2 inhibition.Neoplasia (New York, N.Y.) · 2025Article
- Article
- The intrinsically disordered regions of organellophagy receptors are interchangeable and control organelle fragmentation, ER-phagy and mitophagy flux.Nature cell biology · 2025Article
- Endocytome profiling uncovers cell-surface protein dynamics underlying neuronal connectivity.bioRxiv : the preprint server for biology · 2025Article
- N-palmitoyl glycine mediates depression-associated atrial fibrillation via Man1a2-dependent autophagy and NRAP dysregulation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Allosteric Modulation of GCase Enhances Lysosomal Activity and Reduces ER Stress in GCase-Related Disorders.International journal of molecular sciences · 2025Article
- Orchestration of SARS-CoV-2 Nsp4 and host cell ESCRT proteins induces morphological changes of the endoplasmic reticulum.Molecular biology of the cell · 2025Article
- Glycosylation Regulation by TMEM230 in Aging and Autoimmunity.International journal of molecular sciences · 2025Article
- CNX:FAM134B-driven ERLAD of ATZ polymers proceeds via enhanced formation of VAPA:ORP1L:RAB7 contact sites between ER and endolysosomes.Autophagy reports · 2025Article
- FAM134B in Cellular Homeostasis: Bridging Endoplasmic Reticulum-Phagy to Human Diseases.International journal of biological sciences · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Efficient degradation of by-products of protein biogenesis maintains cellular fitness. Strikingly, the major biosynthetic compartment in eukaryotic cells, the endoplasmic reticulum (ER), lacks degradative machineries. Misfolded proteins in the ER are translocated to the cytosol for proteasomal degradation via ER-associated degradation (ERAD). Alternatively, they are segregated in ER subdomains that are shed from the biosynthetic compartment and are delivered to endolysosomes under control of ER-phagy receptors for ER-to-lysosome-associated degradation (ERLAD). Demannosylation of N-linked oligosaccharides targets terminally misfolded proteins for ERAD. How misfolded proteins are eventually marked for ERLAD is not known. Here, we show for ATZ and mutant Pro-collagen that cycles of de-/re-glucosylation of selected N-glycans and persistent association with Calnexin (CNX) are required and sufficient to mark ERAD-resistant misfolded proteins for FAM134B-driven lysosomal delivery. In summary, we show that mannose and glucose processing of N-glycans are triggering events that target misfolded proteins in the ER to proteasomal (ERAD) and lysosomal (ERLAD) clearance, respectively, regulating protein quality control in eukaryotic cells.
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