ArticleMolecular biology of the cell2002
Probing for membrane domains in the endoplasmic reticulum: retention and degradation of unassembled MHC class I molecules.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 51 citations in OpenAlex.
- Immunoglobulin-Like Receptors and Their Impact on Wiring of Brain Synapses.Annual review of genetics · 2018Review
- Visualizing Mutation-Specific Differences in the Trafficking-Deficient Phenotype of Kv11.1 Proteins Linked to Long QT Syndrome Type 2.Frontiers in physiology · 2018Article
- PirB regulates asymmetries in hippocampal circuitry.PloS one · 2017Article
- Article
- Adopting the rapamycin trapping assay to track the trafficking of murine MHC class I alleles, H-2K(b).BMC cell biology · 2015Article
- Single-molecule analyses of fully functional fluorescent protein-tagged follitropin receptor reveal homodimerization and specific heterodimerization with lutropin receptor.Biology of reproduction · 2015Article
- An updated view of the intracellular mechanisms regulating cross-presentation.Frontiers in immunology · 2013Review
- Neuronal major histocompatibility complex class I molecules are implicated in the generation of asymmetries in hippocampal circuitry.The Journal of physiology · 2013Article
- Golgi-situated endoplasmic reticulum α-1, 2-mannosidase contributes to the retrieval of ERAD substrates through a direct interaction with γ-COP.Molecular biology of the cell · 2013Article
- The expression patterns of MHC class I molecules in the developmental human visual system.Neurochemical research · 2013Article
- The major histocompatibility complex and autism spectrum disorder.Developmental neurobiology · 2012Review
- Regulation of CD20 in rituximab-resistant cell lines and B-cell non-Hodgkin lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Article
- Trafficking-deficient hERG K⁺ channels linked to long QT syndrome are regulated by a microtubule-dependent quality control compartment in the ER.American journal of physiology. Cell physiology · 2011Article
- MHCI negatively regulates synapse density during the establishment of cortical connections.Nature neuroscience · 2011Article
- Life and death of a BiP substrate.Seminars in cell & developmental biology · 2010Review
- Pathogen evasion strategies for the major histocompatibility complex class I assembly pathway.Immunology · 2008Review
- Bap31 is an itinerant protein that moves between the peripheral endoplasmic reticulum (ER) and a juxtanuclear compartment related to ER-associated Degradation.Molecular biology of the cell · 2008Article
- Peptide-based interactions with calnexin target misassembled membrane proteins into endoplasmic reticulum-derived multilamellar bodies.Journal of molecular biology · 2008Article
- Measuring rotational diffusion of MHC class I on live cells by polarized FPR.Biophysical chemistry · 2007Article
- Receptor complexes cotransported via polarized endocytic pathways form clusters with distinct organizations.Molecular biology of the cell · 2007Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Quality control of protein biosynthesis requires ER-retention and ER-associated degradation (ERAD) of unassembled/misfolded molecules. Although some evidence exists for the organization of the ER into functionally distinct membrane domains, it is unknown if such domains are involved in the retention and ERAD of unassembled proteins. Here, it is shown that unassembled MHC class I molecules are retained in the ER without accumulating at ER-exit sites or in the ERGIC of beta2m-/- cells. Furthermore, these molecules did not cluster in the ER membrane and appeared to be highly mobile even when ERAD or their association with calnexin were inhibited. However, upon ATP depletion, they were reversibly segregated into an ER membrane domain, distinct from ER exit sites, which included calnexin and COPII, but not the ERGIC marker protein p58. This quality control domain was also observed upon prolonged inhibition of proteasomes. Microtubules were required for its appearance. Segregation of unfolded proteins, ER-resident chaperones, and COPII may be a temporal adaptation to cell stress.
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Registered trials
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.