Pages that link to "Q28217928"
Jump to navigation
Jump to search
The following pages link to Functional and biochemical analysis of a sodium channel beta1 subunit mutation responsible for generalized epilepsy with febrile seizures plus type 1 (Q28217928):
Displaying 50 items.
- Crystallographic insights into sodium-channel modulation by the β4 subunit (Q24310927) (← links)
- Trafficking mechanisms underlying neuronal voltage-gated ion channel localization at the axon initial segment (Q26829715) (← links)
- HDAC1/2-Dependent P0 Expression Maintains Paranodal and Nodal Integrity Independently of Myelin Stability through Interactions with Neurofascins (Q27346711) (← links)
- On the multiple roles of the voltage gated sodium channel β1 subunit in genetic diseases (Q28080803) (← links)
- Sodium channel β subunits: emerging targets in channelopathies (Q28082122) (← links)
- (Q28190181) (redirect page) (← links)
- A deletion in SCN1B is associated with febrile seizures and early-onset absence epilepsy (Q28204457) (← links)
- Functional characterization of the D188V mutation in neuronal voltage-gated sodium channel causing generalized epilepsy with febrile seizures plus (GEFS) (Q28208131) (← links)
- A novel epilepsy mutation in the sodium channel SCN1A identifies a cytoplasmic domain for beta subunit interaction (Q28291611) (← links)
- Slow inactivation of the NaV1.4 sodium channel in mammalian cells is impeded by co-expression of the beta1 subunit (Q28298167) (← links)
- Mice lacking sodium channel beta1 subunits display defects in neuronal excitability, sodium channel expression, and nodal architecture (Q28506321) (← links)
- Voltage-gated Na+ channel beta1 subunit-mediated neurite outgrowth requires Fyn kinase and contributes to postnatal CNS development in vivo (Q28510216) (← links)
- The importance of serine 161 in the sodium channel beta3 subunit for modulation of Na(V)1.2 gating (Q30430912) (← links)
- Modulation of voltage-gated K+ channels by the sodium channel β1 subunit (Q30460758) (← links)
- Localization and targeting of voltage-dependent ion channels in mammalian central neurons. (Q30492681) (← links)
- Axon initial segment dysfunction in a mouse model of genetic epilepsy with febrile seizures plus (Q30495760) (← links)
- Chondrocyte channel transcriptomics: do microarray data fit with expression and functional data? (Q30664498) (← links)
- Cloning and expression of a zebrafish SCN1B ortholog and identification of a species-specific splice variant (Q33290469) (← links)
- Functional reciprocity between Na+ channel Nav1.6 and beta1 subunits in the coordinated regulation of excitability and neurite outgrowth (Q33719761) (← links)
- Organization and maintenance of molecular domains in myelinated axons (Q33726825) (← links)
- Inherited disorders of voltage-gated sodium channels (Q33905815) (← links)
- Comprehensive RNA-Seq expression analysis of sensory ganglia with a focus on ion channels and GPCRs in Trigeminal ganglia (Q35048508) (← links)
- Identification of Navβ1 residues involved in the modulation of the sodium channel Nav1.4. (Q35072592) (← links)
- Mechanisms of sodium channel inactivation (Q35172793) (← links)
- Na Channel β Subunits: Overachievers of the Ion Channel Family (Q35235909) (← links)
- Contrast gain control abnormalities in idiopathic generalized epilepsy. (Q35243852) (← links)
- Voltage-gated Na+ channel β1B: a secreted cell adhesion molecule involved in human epilepsy (Q35538368) (← links)
- Voltage-gated Na+ channels: multiplicity of expression, plasticity, functional implications and pathophysiological aspects (Q35667228) (← links)
- Monogenic idiopathic epilepsies (Q35708106) (← links)
- An emerging role for voltage-gated Na+ channels in cellular migration: regulation of central nervous system development and potentiation of invasive cancers (Q36049612) (← links)
- Sodium channel mutations in epilepsy and other neurological disorders (Q36216288) (← links)
- Identification of the cysteine residue responsible for disulfide linkage of Na+ channel α and β2 subunits (Q36385951) (← links)
- Genes and loci involved in febrile seizures and related epilepsy syndromes (Q36426936) (← links)
- Abnormal neuronal patterning occurs during early postnatal brain development of Scn1b-null mice and precedes hyperexcitability. (Q36545491) (← links)
- Non-conducting functions of voltage-gated ion channels (Q36599917) (← links)
- The immunoglobulin domain of the sodium channel β3 subunit contains a surface-localized disulfide bond that is required for homophilic binding (Q36643487) (← links)
- β1-C121W Is Down But Not Out: Epilepsy-Associated Scn1b-C121W Results in a Deleterious Gain-of-Function (Q36985341) (← links)
- A functional null mutation of SCN1B in a patient with Dravet syndrome (Q37359854) (← links)
- Genetic basis in epilepsies caused by malformations of cortical development and in those with structurally normal brain (Q37523411) (← links)
- Blood DNA methylation pattern is altered in mesial temporal lobe epilepsy (Q37690173) (← links)
- GABRA1 and STXBP1: novel genetic causes of Dravet syndrome (Q37725930) (← links)
- Electrophysiology and beyond: multiple roles of Na+ channel β subunits in development and disease (Q37769877) (← links)
- Epileptogenic ion channel mutations: From bedside to bench and, hopefully, back again (Q37786731) (← links)
- The axon initial segment in nervous system disease and injury (Q37958904) (← links)
- Voltage-gated sodium channels: pharmaceutical targets via anticonvulsants to treat epileptic syndromes (Q38093362) (← links)
- Role of Sodium Channels in Epilepsy (Q38825019) (← links)
- Functional modulation of voltage-dependent sodium channel expression by wild type and mutated C121W-β1 subunit. (Q39166783) (← links)
- Regulation of persistent Na current by interactions between beta subunits of voltage-gated Na channels (Q39881948) (← links)
- Hereditary Inclusion Body Myopathy (HIBM2) (Q39911980) (← links)
- Gating of the shaker potassium channel is modulated differentially by N-glycosylation and sialic acids (Q40043668) (← links)