Self-limited hyperexcitability: functional effect of a familial hemiplegic migraine mutation of the Nav1.1 (SCN1A) Na+ channel.
about
Pain as a channelopathyLow-dose fenfluramine in the treatment of neurologic disorders: experience in Dravet syndromeMolecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channelsGenetic epilepsy syndromes without structural brain abnormalities: clinical features and experimental modelsMigraine headache: a review of the molecular genetics of a common disorderHomeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potentialPhenytoin inhibits the persistent sodium current in neocortical neurons by modifying its inactivation propertiesFunctional Effects of Schizophrenia-Linked Genetic Variants on Intrinsic Single-Neuron Excitability: A Modeling Study.Calcium channels and synaptic transmission in familial hemiplegic migraine type 1 animal models.Axon physiology.Impaired action potential initiation in GABAergic interneurons causes hyperexcitable networks in an epileptic mouse model carrying a human Na(V)1.1 mutationInherited neuronal ion channelopathies: new windows on complex neurological diseases.Increased variability of motor cortical excitability to transcranial magnetic stimulation in migraine: a new clue to an old enigma.A deleterious Nav1.1 mutation selectively impairs telencephalic inhibitory neurons derived from Dravet Syndrome patients.Comparative neuronal differentiation of self-renewing neural progenitor cell lines obtained from human induced pluripotent stem cells.Nonfunctional NaV1.1 familial hemiplegic migraine mutant transformed into gain of function by partial rescue of folding defectsA functional null mutation of SCN1B in a patient with Dravet syndrome.Early-onset familial hemiplegic migraine due to a novel SCN1A mutation.Na+ channelopathies and epilepsy: recent advances and new perspectives.Voltage-gated sodium channels: biophysics, pharmacology, and related channelopathies.Neurological perspectives on voltage-gated sodium channels.Divergent effects of the T1174S SCN1A mutation associated with seizures and hemiplegic migraine.Pearls and pitfalls in genetic studies of migraine.Neuronal calcium signaling: function and dysfunction.Mutational consequences of aberrant ion channels in neurological disorders.Pharmacology of the Nav1.1 domain IV voltage sensor reveals coupling between inactivation gating processes.Animal models of monogenic migraine.Mechanisms of spreading depolarization in vertebrate and insect central nervous systemsThe SCN1A mutation database: updating information and analysis of the relationships among genotype, functional alteration, and phenotype.Migraine genetics: current findings and future lines of research.Loss-of-function KCNH2 mutation in a family with long QT syndrome, epilepsy, and sudden death.Pure haploinsufficiency for Dravet syndrome Na(V)1.1 (SCN1A) sodium channel truncating mutations.Two novel SCN1A mutations identified in families with familial hemiplegic migraine.Pleiotropic effects of schizophrenia-associated genetic variants in neuron firing and cardiac pacemaking revealed by computational modeling.Intrinsic neuronal excitability: implications for health and disease.
P2860
Q24622323-9A523B0D-B492-43B4-87C5-3A3F47C112A3Q26776222-670B737D-B0A4-4EF5-A1D7-DDFBEE78F91CQ26800090-BC994924-1AE5-41B0-8947-ABB65DE2822AQ26861471-6B1116A7-B05A-4F72-8DF8-2C083223C634Q27010458-D531457E-A47D-4174-9602-A5120433B71CQ28080655-1B72BB7D-ABC0-4698-9BD7-922AA2661A72Q28485346-9AACA170-A7C3-4BDB-8756-C7B44E0D853AQ30366617-E45984B0-F19D-489D-82CF-8FCD2EFF1C3AQ33680269-827E936E-0E09-4EB5-A4EB-891B59E6043CQ34181026-65A32751-AF11-435A-9630-8E47B6288954Q34451662-A5A2DA4A-B275-49BD-BEA5-3FA417F2F626Q35226085-6C024D37-BB11-4841-8C0E-2FE1A782C869Q35658690-0D5D2B33-35C2-46C7-8B01-FAB08A4D52A6Q37127359-C048114F-71D6-4A8C-977E-45F2A0E63D79Q37217420-B1A792CB-C219-4DDA-AD55-6A864165317EQ37256074-09CF3B42-F5FD-4F32-A44B-A011CCF0C829Q37359854-8978CE1A-E2E6-43B4-8358-366633B0DB22Q37408962-A7333168-44AB-455D-8322-981883DB36BAQ37960093-ECD5C470-81BA-46DB-B62F-49AD90F0AAA5Q38026557-B1F7DF1A-C52E-4C3D-90D1-4FF3605CC0DCQ38042001-9300C455-6D9D-40F8-A4EA-2232680720F4Q38080592-84B85725-EC91-41C6-92F5-33BD310DEF0FQ38106687-E9048F3B-EBF6-42CC-A29A-84EE839B2ED2Q38179996-0B1DE3FC-99BB-4D5D-B98D-278D79267F7FQ38239544-69B9CB96-E898-47CA-AE94-BB4261E3957FQ38728979-A7AD18DC-B4D2-472B-96AA-5BC9CB92DE29Q38828065-FB7F3522-E68C-4648-A701-03864D06DF68Q38873942-5A2368D5-4EB1-494B-B460-DFF1CD091AACQ39031141-36BCF367-6DAC-4A5A-B6BD-34C8B5F1DA11Q39077188-9D05213C-1D31-450E-A3F0-4302E1883544Q39118099-9989E4D5-1B76-4574-ACF5-54A7B71A3B3DQ39431641-18FC4B40-6674-40F4-B8AB-F8333D5B223EQ45047442-668C70D9-E2E8-4FD2-A519-A54AA361D01EQ50317783-3E2D759A-42B3-4C27-85D4-1CD7D037A914Q50998138-4E644B47-9524-45B3-8B7A-8E2BF766F954
P2860
Self-limited hyperexcitability: functional effect of a familial hemiplegic migraine mutation of the Nav1.1 (SCN1A) Na+ channel.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Self-limited hyperexcitability ...... he Nav1.1 (SCN1A) Na+ channel.
@en
Self-limited hyperexcitability ...... igraine mutation of the Nav1.1
@nl
type
label
Self-limited hyperexcitability ...... he Nav1.1 (SCN1A) Na+ channel.
@en
Self-limited hyperexcitability ...... igraine mutation of the Nav1.1
@nl
prefLabel
Self-limited hyperexcitability ...... he Nav1.1 (SCN1A) Na+ channel.
@en
Self-limited hyperexcitability ...... igraine mutation of the Nav1.1
@nl
P2093
P2860
P1476
Self-limited hyperexcitability ...... he Nav1.1 (SCN1A) Na+ channel.
@en
P2093
Benedetta Terragni
Raffaella Rusconi
Sandrine Cestèle
Silvana Franceschetti
P2860
P304
P356
10.1523/JNEUROSCI.4453-07.2008
P407
P577
2008-07-01T00:00:00Z