ArticleThe EMBO journal2004
Regulation of nicotinic receptor expression by the ubiquitin-proteasome system.
Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 103 citations in OpenAlex.
- Protein networking: nicotinic acetylcholine receptors and their protein-protein-associations.Molecular and cellular biochemistry · 2024Review
- Recombinant cellular model system for human muscle-type nicotinic acetylcholine receptor α1Cell stress & chaperones · 2023Article
- Omega-3 Supplementation Prevents Short-Term High-Fat Diet Effects on theMediators of inflammation · 2021Article
- A Variant in the Nicotinic Acetylcholine Receptor Alpha 3 Subunit Gene Is Associated With Hypertension Risks in Hypogonadic Patients.Frontiers in genetics · 2020Article
- The MX-Helix of Muscle nAChR Subunits Regulates Receptor Assembly and Surface Trafficking.Frontiers in molecular neuroscience · 2020Article
- Potentially repurposable drugs for schizophrenia identified from its interactome.Scientific reports · 2019Article
- Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.Medical & biological engineering & computing · 2017Article
- Cognate Ligand Chaperoning: a Novel Mechanism for the Post-translational Regulation of Neurotransmitter Receptor Biogenesis.Frontiers in cellular neuroscience · 2017Article
- Article
- Nicotinic acetylcholine receptors: upregulation, age-related effects and associations with drug use.Genes, brain, and behavior · 2016Review
- The Intracellular Loop of the Glycine Receptor: It's not all about the Size.Frontiers in molecular neuroscience · 2016Review
- UBXN2A regulates nicotinic receptor degradation by modulating the E3 ligase activity of CHIP.Biochemical pharmacology · 2015Article
- Neuronal gamma-aminobutyric acid (GABA) type A receptors undergo cognate ligand chaperoning in the endoplasmic reticulum by endogenous GABA.Frontiers in cellular neuroscience · 2015Article
- Muscle-specific kinase (MuSK) autoantibodies suppress the MuSK pathway and ACh receptor retention at the mouse neuromuscular junction.The Journal of physiology · 2014Article
- Determinants in the β and δ subunit cytoplasmic loop regulate Golgi trafficking and surface expression of the muscle acetylcholine receptor.The Journal of biological chemistry · 2014Article
- Degeneration of neuromuscular junction in age and dystrophy.Frontiers in aging neuroscience · 2014Review
- Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors.Autophagy · 2014Article
- Habenular expression of rare missense variants of the β4 nicotinic receptor subunit alters nicotine consumption.Frontiers in human neuroscience · 2014Article
- High-affinity nicotinic acetylcholine receptor expression and trafficking abnormalities in psychiatric illness.Psychopharmacology · 2013Review
- Nicotine-modulated subunit stoichiometry affects stability and trafficking of α3β4 nicotinic receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Control of ligand-gated ion channel (LGIC) expression is essential for the formation, maintenance and plasticity of synapses. Treatment of mouse myotubes with proteasome inhibitors increased the number of surface nicotinic acetylcholine receptors (AChRs), indicating LGIC expression is regulated by the ubiquitin-proteasome system (UPS). Elevated surface expression resulted from increased AChR delivery to the plasma membrane and not from decreased turnover from the surface. The rise in AChR trafficking was the direct result of increased assembly of subunits in the endoplasmic reticulum (ER). Because proteasome inhibitors also blocked ER-associated degradation (ERAD) of unassembled AChR subunits, the data indicate that the additional AChRs were assembled from subunits normally targeted for ERAD. Our data show that AChR surface expression is regulated by the UPS through ERAD, whose activity determines oligomeric receptor assembly efficiency.
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What OpenQuestion holds
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.