ArticleThe Journal of biological chemistry2015
Functional Interaction between the Scaffold Protein Kidins220/ARMS and Neuronal Voltage-Gated Na+ Channels.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- A non-canonical ARMS-GABARAP interaction modulates dendritic spine formation and synaptic development.The EMBO journal · 2026Article
- Novel autosomal recessive SINO syndrome-associatedHeliyon · 2024Article
- Transient Receptor Potential Vanilloid 1 Signaling Is Independent on Protein Kinase A Phosphorylation of Ankyrin-Rich Membrane Spanning Protein.Medical sciences (Basel, Switzerland) · 2022Article
- Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.Cell death discovery · 2022Article
- Sodium channel subtypes are differentially localized to pre- and post-synaptic sites in rat hippocampus.The Journal of comparative neurology · 2017Article
- Ankyrin-rich membrane spanning protein as a novel modulator of transient receptor potential vanilloid 1-function in nociceptive neurons.European journal of pain (London, England) · 2017Article
- Single-Molecule Imaging of Nav1.6 on the Surface of Hippocampal Neurons Reveals Somatic Nanoclusters.Biophysical journal · 2016Article
- Nav1.7-A1632G Mutation from a Family with Inherited Erythromelalgia: Enhanced Firing of Dorsal Root Ganglia Neurons Evoked by Thermal Stimuli.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.Frontiers in cellular neuroscience · 2016Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kidins220 (kinase D-interacting substrate of 220 kDa)/ankyrin repeat-rich membrane spanning (ARMS) acts as a signaling platform at the plasma membrane and is implicated in a multitude of neuronal functions, including the control of neuronal activity. Here, we used the Kidins220(-/-) mouse model to study the effects of Kidins220 ablation on neuronal excitability. Multielectrode array recordings showed reduced evoked spiking activity in Kidins220(-/-) hippocampal networks, which was compatible with the increased excitability of GABAergic neurons determined by current-clamp recordings. Spike waveform analysis further indicated an increased sodium conductance in this neuronal subpopulation. Kidins220 association with brain voltage-gated sodium channels was shown by co-immunoprecipitation experiments and Na(+) current recordings in transfected HEK293 cells, which revealed dramatic alterations of kinetics and voltage dependence. Finally, an in silico interneuronal model incorporating the Kidins220-induced Na(+) current alterations reproduced the firing phenotype observed in Kidins220(-/-) neurons. These results identify Kidins220 as a novel modulator of Nav channel activity, broadening our understanding of the molecular mechanisms regulating network excitability.
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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.