Pages that link to "Q24563329"
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The following pages link to Noninactivating voltage-gated sodium channels in severe myoclonic epilepsy of infancy (Q24563329):
Displaying 50 items.
- Sodium channel dysfunction in intractable childhood epilepsy with generalized tonic-clonic seizures (Q24544180) (← links)
- Single-channel properties of human NaV1.1 and mechanism of channel dysfunction in SCN1A-associated epilepsy (Q24684695) (← links)
- SCN1A mutations and epilepsy (Q28249270) (← links)
- Mutation in the neuronal voltage-gated sodium channel SCN1A in familial hemiplegic migraine (Q28264653) (← links)
- Phenytoin inhibits the persistent sodium current in neocortical neurons by modifying its inactivation properties (Q28485346) (← links)
- Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation (Q28587835) (← links)
- Persistent Sodium Current and Its Role in Epilepsy (Q29396058) (← links)
- Understanding Sodium Channel Function and Modulation Using Atomistic Simulations of Bacterial Channel Structures. (Q30392501) (← links)
- Genetics and epilepsy (Q30473411) (← links)
- Increased persistent Na+ current contributes to seizure in the slamdance bang-sensitive Drosophila mutant (Q30502114) (← links)
- Excitability constraints on voltage-gated sodium channels (Q33300128) (← links)
- Inherited disorders of voltage-gated sodium channels (Q33905815) (← links)
- Antiepileptic activity of preferential inhibitors of persistent sodium current (Q34020942) (← links)
- Sodium channelopathy induced by mild axonal trauma worsens outcome after a repeat injury (Q34458292) (← links)
- Na(V)1.7 mutant A863P in erythromelalgia: effects of altered activation and steady-state inactivation on excitability of nociceptive dorsal root ganglion neurons. (Q34585853) (← links)
- Nav 1.1 dysfunction in genetic epilepsy with febrile seizures-plus or Dravet syndrome (Q35375026) (← links)
- Paediatrics: genetic insights and long-term follow-up (Q35994363) (← links)
- Pathophysiological role of omega pore current in channelopathies (Q36022793) (← links)
- Sacred disease secrets revealed: the genetics of human epilepsy (Q36210058) (← links)
- Sodium channel mutations in epilepsy and other neurological disorders (Q36216288) (← links)
- Sodium channel inactivation: molecular determinants and modulation (Q36267779) (← links)
- Genes and loci involved in febrile seizures and related epilepsy syndromes (Q36426936) (← links)
- Nontruncating SCN1A mutations associated with severe myoclonic epilepsy of infancy impair cell surface expression (Q36451955) (← links)
- Role of genetics in the diagnosis and treatment of epilepsy (Q36688976) (← links)
- Physiologic principles underlying ion channelopathies (Q36774694) (← links)
- Divergent sodium channel defects in familial hemiplegic migraine (Q36775272) (← links)
- Epileptogenic channelopathies: experimental models of human pathologies. (Q36850245) (← links)
- Febrile temperatures unmask biophysical defects in Nav1.1 epilepsy mutations supportive of seizure initiation. (Q37343879) (← links)
- CRISPR/Cas9 facilitates investigation of neural circuit disease using human iPSCs: mechanism of epilepsy caused by an SCN1A loss-of-function mutation (Q37347828) (← links)
- Novel SCN3A variants associated with focal epilepsy in children (Q37424570) (← links)
- Epileptogenic ion channel mutations: From bedside to bench and, hopefully, back again (Q37786731) (← links)
- Dravet syndrome: insights from in vitro experimental models. (Q37861268) (← links)
- Molecular and cellular basis: Insights from experimental models of Dravet syndrome (Q37861271) (← links)
- Na+ channelopathies and epilepsy: recent advances and new perspectives. (Q37960093) (← links)
- Genotype phenotype associations across the voltage-gated sodium channel family (Q38243946) (← links)
- Recurrent and Non-Recurrent Mutations of SCN8A in Epileptic Encephalopathy (Q38510101) (← links)
- A single Markov-type kinetic model accounting for the macroscopic currents of all human voltage-gated sodium channel isoforms (Q38597831) (← links)
- Mutation of sodium channel SCN3A in a patient with cryptogenic pediatric partial epilepsy (Q39026830) (← links)
- Modeling Dravet syndrome using induced pluripotent stem cells (iPSCs) and directly converted neurons (Q39138608) (← links)
- Different degrees of loss of function between GEFS+ and SMEI Nav 1.1 missense mutants at the same residue induced by rescuable folding defects (Q39360713) (← links)
- Overexpression of the VSSC-associated CAM, β-2, enhances LNCaP cell metastasis associated behavior (Q39435580) (← links)
- Self-limited hyperexcitability: functional effect of a familial hemiplegic migraine mutation of the Nav1.1 (SCN1A) Na+ channel (Q39960558) (← links)
- From Acupuncture to Interaction between δ-Opioid Receptors and Na (+) Channels: A Potential Pathway to Inhibit Epileptic Hyperexcitability. (Q40191419) (← links)
- Impaired inactivation gate stabilization predicts increased persistent current for an epilepsy-associated SCN1A mutation. (Q40275732) (← links)
- Scn1a missense mutation causes limbic hyperexcitability and vulnerability to experimental febrile seizures (Q40347688) (← links)
- Impaired NaV1.2 function and reduced cell surface expression in benign familial neonatal-infantile seizures. (Q40489715) (← links)
- Ranolazine selectively blocks persistent current evoked by epilepsy‐associated NaV1.1 mutations (Q41121995) (← links)
- A plethora of SCN1A mutations: what can they tell us? (Q41837236) (← links)
- Human stefin B normal and patho-physiological role: molecular and cellular aspects of amyloid-type aggregation of certain EPM1 mutants (Q41840051) (← links)
- The Nav channel bench series: Plasmid preparation (Q41873048) (← links)