ArticleThe Journal of cell biology1998
Dislocation of type I membrane proteins from the ER to the cytosol is sensitive to changes in redox potential.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 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.
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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
55 citing papers in PubMed, 123 citations in OpenAlex.
- Initiation of ERAD by the bifunctional complex of Mnl1/Htm1 mannosidase and protein disulfide isomerase.Nature structural & molecular biology · 2025Article
- Initiation of ERAD by the bifunctional complex of Mnl1 mannosidase and protein disulfide isomerase.bioRxiv : the preprint server for biology · 2024Article
- HCMV US2 co-opts TRC8 to degrade the endoplasmic reticulum-resident protein LMAN2L.The Journal of general virology · 2024Article
- DNA damage and transcription stress cause ATP-mediated redesign of metabolism and potentiation of anti-oxidant buffering.Nature communications · 2019Article
- How Are Proteins Reduced in the Endoplasmic Reticulum?Trends in biochemical sciences · 2018Review
- Thiol-reducing agents prevent sulforaphane-induced growth inhibition in ovarian cancer cells.Food & nutrition research · 2017Article
- Heme-independent Redox Sensing by the Heme-Nitric Oxide/Oxygen-binding Protein (H-NOX) from Vibrio cholerae.The Journal of biological chemistry · 2016Article
- Article
- Cyclophilin C Participates in the US2-Mediated Degradation of Major Histocompatibility Complex Class I Molecules.PloS one · 2015Article
- Porcine reproductive and respiratory syndrome (PRRS): an immune dysregulatory pandemic.Immunologic research · 2014Review
- CD4 and BST-2/tetherin proteins retro-translocate from endoplasmic reticulum to cytosol as partially folded and multimeric molecules.The Journal of biological chemistry · 2014Article
- Article
- The human selenoprotein VCP-interacting membrane protein (VIMP) is non-globular and harbors a reductase function in an intrinsically disordered region.The Journal of biological chemistry · 2012Article
- Endoplasmic reticulum-dependent redox reactions control endoplasmic reticulum-associated degradation and pathogen entry.Antioxidants & redox signaling · 2012Review
- Role of the ubiquitin-like protein Urm1 as a noncanonical lysine-directed protein modifier.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Protein disulphide isomerase is required for signal peptide peptidase-mediated protein degradation.The EMBO journal · 2010Article
- Physical and functional interaction of transmembrane thioredoxin-related protein with major histocompatibility complex class I heavy chain: redox-based protein quality control and its potential relevance to immune responses.Molecular biology of the cell · 2009Article
- Dislocation of HMG-CoA reductase and Insig-1, two polytopic endoplasmic reticulum proteins, en route to proteasomal degradation.Molecular biology of the cell · 2009Article
- Cln6 mutants associated with neuronal ceroid lipofuscinosis are degraded in a proteasome-dependent manner.Bioscience reports · 2009Article
- TRAM1 participates in human cytomegalovirus US2- and US11-mediated dislocation of an endoplasmic reticulum membrane glycoprotein.The Journal of biological chemistry · 2009Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human cytomegalovirus (HCMV) gene products US2 and US11 dislocate major histocompatibility class I heavy chains from the ER and target them for proteasomal degradation in the cytosol. The dislocation reaction is inhibited by agents that affect intracellular redox potential and/or free thiol status, such as diamide and N-ethylmaleimide. Subcellular fractionation experiments indicate that this inhibition occurs at the stage of discharge from the ER into the cytosol. The T cell receptor alpha (TCR alpha) chain is also degraded by a similar set of reactions, yet in a manner independent of virally encoded gene products. Diamide and N-ethylmaleimide likewise inhibit the dislocation of the full-length TCR alpha chain from the ER, as well as a truncated, mutant version of TCR alpha chain that lacks cysteine residues. Cytosolic destruction of glycosylated, ER-resident type I membrane proteins, therefore, requires maintenance of a proper redox potential for the initial step of removal of the substrate from the ER environment.
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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.