ArticleMolecular brain2016
RIC-3 expression and splicing regulate nAChR functional expression.
Article in Molecular brain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Disruptions in RNA Splicing: A Key Regulator of Cognitive Impairment in Perioperative Neurocognitive Disorders.Neuroscience bulletin · 2026Review
- Genetic and neuro-epigenetic effects of divergent artificial selection for feather pecking behaviour in chickens.BMC genomics · 2024Article
- Unraveling the molecular interactions between α7 nicotinic receptor and a RIC3 variant associated with backward speech.Cellular and molecular life sciences : CMLS · 2024Article
- Generation of Mutants from the 57B Region ofGenes · 2023Article
- Two residues determine nicotinic acetylcholine receptor requirement for RIC-3.Protein science : a publication of the Protein Society · 2023Article
- Functional α7 nicotinic receptors in human airway smooth muscle increase intracellular calcium concentration and contractility in asthmatics.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Binding motif for RIC-3 chaperon protein in serotonin type 3A receptors.The Journal of general physiology · 2023Article
- Different efficiency of auxiliary/chaperone proteins to promote the functional reconstitution of honeybee glutamate and acetylcholine receptors in Xenopus laevis oocytes.Insect molecular biology · 2022Article
- Speculation on How RIC-3 and Other Chaperones Facilitate α7 Nicotinic Receptor Folding and Assembly.Molecules (Basel, Switzerland) · 2022Review
- Prognostic analysis of m6A-related genes as potential biomarkers in idiopathic pulmonary fibrosis.Frontiers in genetics · 2022Article
- Neuronal Menin Overexpression Rescues Learning and Memory Phenotype in CA1-Specific α7 nAChRs KD Mice.Cells · 2021Article
- Neuroinflammation Modulation via α7 Nicotinic Acetylcholine Receptor and Its Chaperone, RIC-3.Molecules (Basel, Switzerland) · 2021Review
- Nicotinic α7 acetylcholine receptor (α7nAChR) in human airway smooth muscle.Archives of biochemistry and biophysics · 2021Article
- Multidimensional Intersection of Nicotine, Gene Expression, and Behavior.Frontiers in behavioral neuroscience · 2021Article
- RIC3, the cholinergic anti-inflammatory pathway, and neuroinflammation.International immunopharmacology · 2020Article
- Serine residues in the α4 nicotinic acetylcholine receptor subunit regulate surface α4β2Biochemical pharmacology · 2019Article
- Functional Consequences of CHRNA7 Copy-Number Alterations in Induced Pluripotent Stem Cells and Neural Progenitor Cells.American journal of human genetics · 2017Article
- Regulation of RIC-3 and of nAChR expression.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe nicotinic acetylcholine receptors form a large and diverse family of acetylcholine gated ion channels having diverse roles in the central nervous system. Maturation of nicotinic acetylcholine receptors is a complex and inefficient process requiring assistance from multiple cellular factors including RIC-3, a functionally conserved endoplasmic reticulum-resident protein and nicotinic acetylcholine receptor-specific chaperone. In mammals and in Drosophila melanogaster RIC-3 is alternatively spliced to produce multiple isoforms.
resultsWe used electrophysiological analysis in Xenopus laevis oocytes, in situ hybridization, and quantitative real-time polymerase chain reaction assays to investigate regulation of RIC-3's expression and splicing and its effects on the expression of three major neuronal nicotinic acetylcholine receptors. We found that RIC-3 expression level and splicing affect nicotinic acetylcholine receptor functional expression and that two conserved RIC-3 isoforms express in the brain differentially. Moreover, in immune cells RIC-3 expression and splicing are regulated by inflammatory signals.
conclusionsRegulation of expression level and splicing of RIC-3 in brain and in immune cells following inflammation enables regulation of nicotinic acetylcholine receptor functional expression. Specifically, in immune cells such regulation via effects on α7 nicotinic acetylcholine receptor, known to function in the cholinergic anti-inflammatory pathway, may have a role in neuroinflammatory diseases.
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