scholarly article | Q13442814 |
review article | Q7318358 |
P50 | author | Donghua Zou | Q47879234 |
P2093 | author name string | Hai Xiao | |
Yuan Wu | |||
Yiqing Huang | |||
Xingyue Qin | |||
Yuan Nong | |||
P2860 | cites work | First mutation in the voltage-gated Nav1.1 subunit gene SCN1A with co-occurring familial hemiplegic migraine and epilepsy. | Q51819010 |
Familial hemiplegic migraine due to L263V SCN1A mutation: Discordance for epilepsy between two kindreds from Douro Valley | Q57949541 | ||
PRRT2 mutations cause hemiplegic migraine | Q85217137 | ||
PRRT2 mutation causes benign familial infantile convulsions | Q85217152 | ||
Mutations of SCN1A, encoding a neuronal sodium channel, in two families with GEFS+2 | Q22253421 | ||
Haploinsufficiency of ATP1A2 encoding the Na+/K+ pump alpha2 subunit associated with familial hemiplegic migraine type 2 | Q24293004 | ||
Exome sequencing identifies truncating mutations in PRRT2 that cause paroxysmal kinesigenic dyskinesia | Q24297970 | ||
A human protein-protein interaction network: a resource for annotating the proteome | Q24324450 | ||
De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy | Q24533495 | ||
Comorbidity between headache and epilepsy in a pediatric headache center | Q24596020 | ||
Calcium channels and migraine | Q26859229 | ||
Genetic epilepsy syndromes without structural brain abnormalities: clinical features and experimental models | Q26861471 | ||
Structure-function of proteins interacting with the α1 pore-forming subunit of high-voltage-activated calcium channels | Q26864613 | ||
Novel mutations in the Na+, K+-ATPase pump gene ATP1A2 associated with familial hemiplegic migraine and benign familial infantile convulsions | Q28204791 | ||
Mutations of sodium channel alpha subunit type 1 (SCN1A) in intractable childhood epilepsies with frequent generalized tonic-clonic seizures | Q28207332 | ||
A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression | Q28248603 | ||
SCN1A mutations and epilepsy | Q28249270 | ||
Variability of familial hemiplegic migraine with novel A1A2 Na+/K+-ATPase variants | Q28263111 | ||
New CACNA1A gene mutation in a case of familial hemiplegic migraine with status epilepticus | Q28270794 | ||
Sodium channels, inherited epilepsy, and antiepileptic drugs | Q28305262 | ||
PRRT2 mutations in familial infantile seizures, paroxysmal dyskinesia, and hemiplegic migraine. | Q30528873 | ||
PRRT2 gene mutations: from paroxysmal dyskinesia to episodic ataxia and hemiplegic migraine | Q30528874 | ||
CaV 2.1 ablation in cortical interneurons selectively impairs fast-spiking basket cells and causes generalized seizures | Q30558547 | ||
CaV2.1 channelopathies | Q33537218 | ||
Biphasic direct current shift, haemoglobin desaturation and neurovascular uncoupling in cortical spreading depression | Q33773471 | ||
Human epilepsy associated with dysfunction of the brain P/Q-type calcium channel | Q34091858 | ||
Identification of PRRT2 as the causative gene of paroxysmal kinesigenic dyskinesias | Q34236213 | ||
Mechanisms of spreading depression and hypoxic spreading depression-like depolarization | Q34294064 | ||
Impaired action potential initiation in GABAergic interneurons causes hyperexcitable networks in an epileptic mouse model carrying a human Na(V)1.1 mutation | Q34451662 | ||
Chronic disorders with episodic manifestations: focus on epilepsy and migraine | Q34590975 | ||
PRRT2 mutations cause benign familial infantile epilepsy and infantile convulsions with choreoathetosis syndrome | Q35671504 | ||
Mutations in the gene PRRT2 cause paroxysmal kinesigenic dyskinesia with infantile convulsions. | Q35906678 | ||
Sodium channel mutations in epilepsy and other neurological disorders | Q36216288 | ||
Two novel alleles of tottering with distinct Ca(v)2.1 calcium channel neuropathologies | Q37079538 | ||
Epilepsy, hippocampal sclerosis and febrile seizures linked by common genetic variation around SCN1A. | Q37200320 | ||
Nonfunctional NaV1.1 familial hemiplegic migraine mutant transformed into gain of function by partial rescue of folding defects | Q37256074 | ||
Optical current source density analysis in hippocampal organotypic culture shows that spreading depression occurs with uniquely reversing currents. | Q37266046 | ||
Screening of CACNA1A and ATP1A2 genes in hemiplegic migraine: clinical, genetic, and functional studies. | Q37398107 | ||
Genetic and functional characterisation of the P/Q calcium channel in episodic ataxia with epilepsy | Q37692702 | ||
Sodium channel SCN1A and epilepsy: mutations and mechanisms | Q37787324 | ||
Na+, K+-ATPase: functions in the nervous system and involvement in neurologic disease | Q37829577 | ||
Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management | Q37860502 | ||
Neuronal P/Q-type calcium channel dysfunction in inherited disorders of the CNS. | Q37976377 | ||
Chaos and commotion in the wake of cortical spreading depression and spreading depolarizations | Q38214404 | ||
The role of calcium channel mutations in human epilepsy. | Q38246527 | ||
PRRT2: a major cause of infantile epilepsy and other paroxysmal disorders of childhood | Q38246531 | ||
Rescuable folding defective NaV1.1 (SCN1A) mutants in epilepsy: properties, occurrence, and novel rescuing strategy with peptides targeted to the endoplasmic reticulum | Q38921427 | ||
Pure haploinsufficiency for Dravet syndrome Na(V)1.1 (SCN1A) sodium channel truncating mutations | Q39431641 | ||
Synaptic gain-of-function effects of mutant Cav2.1 channels in a mouse model of familial hemiplegic migraine are due to increased basal [Ca2+]i | Q39806572 | ||
Ranolazine selectively blocks persistent current evoked by epilepsy‐associated NaV1.1 mutations | Q41121995 | ||
Abnormal cortical synaptic transmission in CaV2.1 knockin mice with the S218L missense mutation which causes a severe familial hemiplegic migraine syndrome in humans | Q41292581 | ||
CACNA1A haploinsufficiency causes cognitive impairment, autism and epileptic encephalopathy with mild cerebellar symptoms | Q42064482 | ||
CaV2.1 (P/Q channel) interaction with synaptic proteins is essential for depolarization-evoked release | Q43056190 | ||
CACNA1A variants may modify the epileptic phenotype of Dravet syndrome. | Q43851698 | ||
Glutamate transporter coupling to Na,K-ATPase. | Q45954183 | ||
Cortical spreading depression modulates synaptic transmission of the rat lateral amygdala | Q46644693 | ||
A novel ATP1A2 gene mutation in familial hemiplegic migraine and epilepsy | Q46665221 | ||
Electroencephalographic changes and seizures in familial hemiplegic migraine patients with the CACNA1A gene S218L mutation | Q46722961 | ||
Absence-like seizures and their pharmacological profile in tottering-6j mice | Q47971094 | ||
Familial hemiplegic migraine type-1 mutated cav2.1 calcium channels alter inhibitory and excitatory synaptic transmission in the lateral superior olive of mice | Q48157176 | ||
Partial epilepsy with antecedent febrile seizures and seizure aggravation by antiepileptic drugs: associated with loss of function of Na(v) 1.1. | Q48164995 | ||
Functional characterization of a novel C-terminal ATP1A2 mutation causing hemiplegic migraine and epilepsy. | Q48621714 | ||
Dysfunction of the brain calcium channel CaV2.1 in absence epilepsy and episodic ataxia | Q48810235 | ||
P275 | copyright license | Creative Commons Attribution-NonCommercial 3.0 Unported | Q18810331 |
P6216 | copyright status | copyrighted | Q50423863 |
P407 | language of work or name | English | Q1860 |
P921 | main subject | migraine | Q133823 |
P304 | page(s) | 1175-1179 | |
P577 | publication date | 2017-04-24 | |
P1433 | published in | Neuropsychiatric Disease and Treatment | Q15716332 |
P1476 | title | The genetic relationship between epilepsy and hemiplegic migraine | |
P478 | volume | 13 |
Search more.