ArticleProceedings of the National Academy of Sciences of the United States of America2017
FGF14 is a regulator of KCNQ2/3 channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Genotype and Age at Onset Drive Vermis Atrophy in CACNA1A- and GAA-FGF14-related Ataxias.Cerebellum (London, England) · 2026Article
- In Vivo Expression of an SCA27A-LinkedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Depleting retinoic acid synthesis in the nucleus accumbens shell produces a protective phenotype for emotional reactivity and drug-taking in rats.Psychopharmacology · 2026Article
- GAA-FGF14 Expansions and CACNA1A Variants: Phenotypic Overlap and Diagnostic Implications.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Loss of intracellular FGF14 (iFGF14) increases excitability of mature hippocampal pyramidal neurons.The Journal of general physiology · 2025Article
- Article
- Enhanced motivated behavior mediated by pharmacological targeting of the FGF14/NaNature communications · 2025Article
- Parvalbumin interneuron impairment causes synaptic transmission deficits and seizures in SCN8A developmental and epileptic encephalopathy.JCI insight · 2024Article
- Identification and characterisation of pathogenic and non-pathogenic FGF14 repeat expansions.Nature communications · 2024Article
- Spinocerebellar ataxia 27B: a frequent and slowly progressive autosomal-dominant cerebellar ataxia-experience from an Italian cohort.Journal of neurology · 2024Article
- Live imaging of excitable axonal microdomains in ankyrin-G-GFP mice.bioRxiv : the preprint server for biology · 2024Article
- A Developmental Switch in Cholinergic Mechanisms of Modulation in the Medial Nucleus of the Trapezoid Body.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Downbeat nystagmus: a clinical and pathophysiological review.Frontiers in neurology · 2024Review
- Fibroblast growth factor signaling in axons: from development to disease.Cell communication and signaling : CCS · 2023Review
- Fibroblast growth factor 13-mediated regulation of medium spiny neuron excitability and cocaine self-administration.Frontiers in neuroscience · 2023Article
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- Glycogen Synthase Kinase 3: Ion Channels, Plasticity, and Diseases.International journal of molecular sciences · 2022Review
- TheReports of biochemistry & molecular biology · 2022Article
- Poly-dipeptides produced fromProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Exploring the Genomic Patterns in Human and Mouse Cerebellums Via Single-Cell Sequencing and Machine Learning Method.Frontiers in genetics · 2022Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
KCNQ2/3 (Kv7.2/7.3) channels and voltage-gated sodium channels (VGSCs) are enriched in the axon initial segment (AIS) where they bind to ankyrin-G and coregulate membrane potential in central nervous system neurons. The molecular mechanisms supporting coordinated regulation of KCNQ and VGSCs and the cellular mechanisms governing KCNQ trafficking to the AIS are incompletely understood. Here, we show that fibroblast growth factor 14 (FGF14), previously described as a VGSC regulator, also affects KCNQ function and localization. FGF14 knockdown leads to a reduction of KCNQ2 in the AIS and a reduction in whole-cell KCNQ currents. FGF14 positively regulates KCNQ2/3 channels in a simplified expression system. FGF14 interacts with KCNQ2 at a site distinct from the FGF14-VGSC interaction surface, thus enabling the bridging of Na
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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.