ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
The neural cell adhesion molecule regulates cell-surface delivery of G-protein-activated inwardly rectifying potassium channels via lipid rafts.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 94 citations in OpenAlex.
- Interaction with stomatin directs human proton channels into cholesterol-dependent membrane domains.Biophysical journal · 2024Article
- Direct modulation of G protein-gated inwardly rectifying potassium (GIRK) channels.Frontiers in physiology · 2024Review
- Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity.Cell stem cell · 2022Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Structural insights into GIRK2 channel modulation by cholesterol and PIPCell reports · 2021Article
- New Partners Identified by Mass Spectrometry Assay Reveal Functions of NCAM2 in Neural Cytoskeleton Organization.International journal of molecular sciences · 2021Article
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Attenuated palmitoylation of serotonin receptor 5-HT1A affects receptor function and contributes to depression-like behaviors.Nature communications · 2019Article
- Dual activation of neuronal G protein-gated inwardly rectifying potassium (GIRK) channels by cholesterol and alcohol.Scientific reports · 2017Article
- Intracellular transport and cell surface delivery of the neural cell adhesion molecule (NCAM).Bioarchitecture · 2015Review
- Lipid rafts in neurodegeneration and neuroprotection.Molecular neurobiology · 2014Review
- Ceramide function in the brain: when a slight tilt is enough.Cellular and molecular life sciences : CMLS · 2013Review
- Are NCAM deficient mice an animal model for schizophrenia?Frontiers in behavioral neuroscience · 2012Article
- Functional consequences of the interactions among the neural cell adhesion molecule NCAM, the receptor tyrosine kinase TrkB, and the inwardly rectifying K+ channel KIR3.3.The Journal of biological chemistry · 2010Article
- Do caveolae have a role in the fidelity and dynamics of receptor activation of G-protein-gated inwardly rectifying potassium channels?The Journal of biological chemistry · 2010Article
- Lipid microdomains and the regulation of ion channel function.The Journal of physiology · 2010Review
- Article
- Cholesterol and ion channels.Sub-cellular biochemistry · 2010Review
- Cholesterol and Kir channels.IUBMB life · 2009Review
- Acid-sensing ion channel 3 (ASIC3) cell surface expression is modulated by PSD-95 within lipid rafts.American journal of physiology. Cell physiology · 2008Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice deficient in the neural cell adhesion molecule (NCAM) exhibit increased anxiety and anxiolytic sensitivity to serotonin 5-HT1A receptor agonists. Here, we investigate the relationship between NCAM and 5-HT1A receptor signaling pathways modulating G-protein-activated inwardly rectifying K+ (Kir3) channels. When studying this relationship in cultured hippocampal neurons, we observed that in cells from NCAM-deficient mice, inwardly rectifying K+ (Kir3) currents were increased compared with wild-type controls. Analysis of this modulatory mechanism in Xenopus oocytes and Chinese hamster ovary (CHO) cells revealed that the recombinantly expressed major transmembrane isoforms NCAM140 and NCAM180 specifically reduced inward currents generated by neuronal Kir3.1/3.2 and Kir3.1/3.3 but not by cardiac Kir3.1/3.4 channels. Using fluorescence measurements and surface biotinylation assays, we show that this effect was caused by a reduced surface localization of Kir3 channels. Furthermore, expression of flag-tagged Kir3 channels in cultured neurons of NCAM-deficient mice resulted in a higher transport of these channels into neurites and a higher cell-surface localization compared with wild-type neurons. Neuronal Kir3 channels and NCAM isoforms are associated with cholesterol-rich microdomains (lipid rafts) in CHO cells and in isolated brain membranes. Mutational and pharmacological disruption of the lipid raft association of NCAM140 normalizes surface delivery of channels. We conclude that the transmembrane isoforms of NCAM reduce the transport of Kir3 channels to the cell surface via lipid rafts. Thus, regulation of Kir3 channel activity by NCAM may represent a novel mechanism controlling long-term excitability of neurons.
Indexed as
Identifiers
12177211PMC6757893W1564531279What 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.