SCN9A Epileptic Encephalopathy Mutations Display a Gain-of-function Phenotype and Distinct Sensitivity to Oxcarbazepine
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Title
SCN9A Epileptic Encephalopathy Mutations Display a Gain-of-function Phenotype and Distinct Sensitivity to Oxcarbazepine
Authors
Keywords
Voltage-gated sodium channel, <em class="EmphasisTypeItalic ">SCN9A</em>, Epilepsy, Electrophysiological function, Oxcarbazepine, Sensitivity
Journal
Neuroscience Bulletin
Volume -, Issue -, Pages -
Publisher
Springer Science and Business Media LLC
Online
2019-08-01
DOI
10.1007/s12264-019-00413-5
References
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Note: Only part of the references are listed.- Variable epilepsy phenotypes associated with heterozygous mutation in the SCN9A gene: report of two cases
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- Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7
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- Q10R mutation in SCN9A gene is associated with generalized epilepsy with febrile seizures plus
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- Expression and Role of Voltage-Gated Sodium Channels in Human Dorsal Root Ganglion Neurons with Special Focus on Nav1.7, Species Differences, and Regulation by Paclitaxel
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- (2010) Nicholas J. Hargus et al. NEUROBIOLOGY OF DISEASE
- The Amino Acid Motif L/IIxxFE Defines a Novel Actin-Binding Sequence in PDZ-RhoGEF
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- A Role of SCN9A in Human Epilepsies, As a Cause of Febrile Seizures and As a Potential Modifier of Dravet Syndrome
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- Mutation of sodium channel SCN3A in a patient with cryptogenic pediatric partial epilepsy
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- Divergent sodium channel defects in familial hemiplegic migraine
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