ArticleMolecular biology of the cell2001
A novel quality control compartment derived from the endoplasmic reticulum.
Article in Molecular biology of the cell, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
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Who cites it
94 citing papers in PubMed, 189 citations in OpenAlex.
- ER-to-Golgi transport machinery promotes the excessive cargo-triggered unfolded protein response in C. elegans.PLoS genetics · 2026Article
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- Transgenic expression of endoplasmic reticulum proteins inmicroPublication biology · 2025Article
- Endoplasmic Reticulum Stress in Gliomas: Exploiting a Dual-Effect Dysfunction through Chemical Pharmaceutical Compounds and Natural Derivatives for Therapeutical Uses.International journal of molecular sciences · 2024Review
- Endoplasmic reticulum network heterogeneity guides diffusive transport and kinetics.Biophysical journal · 2023Article
- COP I and II dependent trafficking controls ER-associated degradation in mammalian cells.iScience · 2023Article
- Evidence for Recombinant GRP78, CALR, PDIA3 and GPI as Mediators of Genetic Instability in Human CD34+ Cells.Cancers · 2022Article
- Delivery of phosphatidylethanolamine blunts stress in hepatoma cells exposed to elevated palmitate by targeting the endoplasmic reticulum.Cell death discovery · 2020Article
- The Human Cytomegalovirus Nonstructural Glycoprotein UL148 Reorganizes the Endoplasmic Reticulum.mBio · 2019Article
- The enigmatic ATP supply of the endoplasmic reticulum.Biological reviews of the Cambridge Philosophical Society · 2019Review
- Endoplasmic reticulum stress signalling - from basic mechanisms to clinical applications.The FEBS journal · 2019Review
- Endoplasmic reticulum-retained podocin mutants are massively degraded by the proteasome.The Journal of biological chemistry · 2018Article
- Mannosidase activity of EDEM1 and EDEM2 depends on an unfolded state of their glycoprotein substrates.Communications biology · 2018Article
- Visualizing Mutation-Specific Differences in the Trafficking-Deficient Phenotype of Kv11.1 Proteins Linked to Long QT Syndrome Type 2.Frontiers in physiology · 2018Article
- Protein Quality Control in Health and Disease.Cold Spring Harbor perspectives in biology · 2017Review
- The Emerging Roles of Early Protein Folding Events in the Secretory Pathway in the Development of Neurodegenerative Maladies.Frontiers in neuroscience · 2017Review
- mTORC1 inhibitor rapamycin and ER stressor tunicamycin induce differential patterns of ER-mitochondria coupling.Scientific reports · 2016Article
- Heterozygous Loss-of-Function SEC61A1 Mutations Cause Autosomal-Dominant Tubulo-Interstitial and Glomerulocystic Kidney Disease with Anemia.American journal of human genetics · 2016Article
- N-Glycan-based ER Molecular Chaperone and Protein Quality Control System: The Calnexin Binding Cycle.Traffic (Copenhagen, Denmark) · 2016Review
- Role of Carbonyl Modifications on Aging-Associated Protein Aggregation.Scientific reports · 2016Article
34 more citing papers are in PubMed but not listed here.
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
Degradation of proteins that, because of improper or suboptimal processing, are retained in the endoplasmic reticulum (ER) involves retrotranslocation to reach the cytosolic ubiquitin-proteasome machinery. We found that substrates of this pathway, the precursor of human asialoglycoprotein receptor H2a and free heavy chains of murine class I major histocompatibility complex (MHC), accumulate in a novel preGolgi compartment that is adjacent to but not overlapping with the centrosome, the Golgi complex, and the ER-to-Golgi intermediate compartment (ERGIC). On its way to degradation, H2a associated increasingly after synthesis with the ER translocon Sec61. Nevertheless, it remained in the secretory pathway upon proteasomal inhibition, suggesting that its retrotranslocation must be tightly coupled to the degradation process. In the presence of proteasomal inhibitors, the ER chaperones calreticulin and calnexin, but not BiP, PDI, or glycoprotein glucosyltransferase, concentrate in the subcellular region of the novel compartment. The "quality control" compartment is possibly a subcompartment of the ER. It depends on microtubules but is insensitive to brefeldin A. We discuss the possibility that it is also the site for concentration and retrotranslocation of proteins that, like the mutant cystic fibrosis transmembrane conductance regulator, are transported to the cytosol, where they form large aggregates, the "aggresomes."
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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.