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SCN8A encodes a member of the sodium channel alpha subunit gene family. Additionally we are shipping SCN8A Proteins (11) and SCN8A Kits (1) and many more products for this protein.
Showing 10 out of 45 products:
Human Monoclonal SCN8A Primary Antibody for IF, WB - ABIN396453
Wang, Zhang, Liu, Shao, Wei, Li, Ji, Yang, Wang, Liu, Wan, Li, Xu, Feng, He, He: Genetic polymorphisms in the SCN8A gene are associated with suicidal behavior in psychiatric disorders in the Chinese population. in The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry 2010
Show all 5 references for ABIN396453
Human Polyclonal SCN8A Primary Antibody for IHC, WB - ABIN350858
De Repentigny, Cuotue, Pool, Bernier, Girard, Vidal, Kothary: Pathological and genetic analysis of the degenerating muscle (dmu) mouse: a new allele of Scn8a. in Human molecular genetics 2001
Show all 5 references for ABIN350858
Human Monoclonal SCN8A Primary Antibody for IF, WB - ABIN2476430
Ogiwara, Miyamoto, Morita, Atapour, Mazaki, Inoue, Takeuchi, Itohara, Yanagawa, Obata, Furuichi, Hensch, Yamakawa: Nav1.1 localizes to axons of parvalbumin-positive inhibitory interneurons: a circuit basis for epileptic seizures in mice carrying an Scn1a gene mutation. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2007
Dog (Canine) Polyclonal SCN8A Primary Antibody for WB - ABIN2776199
Martin, Tang, Papale, Yu, Catterall, Escayg: The voltage-gated sodium channel Scn8a is a genetic modifier of severe myoclonic epilepsy of infancy. in Human molecular genetics 2007
the calpain-dependent cleavage of Nav1.6 channels expressed in human embryonic kidney (HEK) 293 cells caused the upregulation of I(NaP)
Our study establishes SCN8A as a novel gene in which a recurrent mutation causes BFIS/ICCA (show PRRT2 Antibodies), expanding the clinical-genetic spectrum of combined epileptic and dyskinetic syndromes.
Human Nav1.6 channels generate larger resurgent currents than human Nav1.1 (show SCN1A Antibodies) channels, but the SCN4B (show SCN4B Antibodies)-derived Navbeta4 (show SCN4B Antibodies) peptide does not protect either isoform from use-dependent reduction.
These data strengthen previous findings linking gain-of-function mutations of SCN8A with EIEE and demonstrate the importance of functional testing in establishing the pathogenicity of de novo mutations.
Expression profiling of SCN8A and NDUFC2 (show NDUFC2 Antibodies) genes in colorectal carcinoma is reported. There was no NDUFC2 (show NDUFC2 Antibodies) differential expression in colorectal carcinoma.
Epileptic encephalopathy related to mutations in the SCN8A genes.
SCN8A encephalopathy presents in infancy with multiple seizure types.
The results of this study suggested that SCN8A mutation cause early onset epilepsy and intellectual disability.
identified the PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies) pathway, the cell-cycle regulator (show CDKN2A Antibodies) Wee1 kinase (show WEE1 Antibodies), and protein kinase C (PKC (show PKC Antibodies)) as prospective regulatory nodes of neuronal excitability through modulation of the FGF14 (show FGF14 Antibodies):Nav1.6 complex.
Data support the contribution of gain-of-function mutations of Nav1.6 (de novo variant p.Thr767Ile) that increase excitatory pyramidal neuron excitability
the presences of Nav1.1 (show SCN1A Antibodies), Nav1.6, Navbeta1 and Navbeta3 mRNA and their reduced levels in rat SAN during aging.
This study demonstrates that Nav channel expression in lumbar motoneurons is altered after SCI, and it shows a tight relationship between the calpain-dependent proteolysis of Nav1.6 channels, the upregulation of I(NaP (show CTNNBL1 Antibodies)) and spastici
the role of Nav1.6 in general anesthesia using two mouse mutants with reduced activity of Nav1.6, was examined.
observed increased hippocampal pyramidal cell excitability in heterozygous and homozygous Scn8a-R1627H mutants, and decreased interneuron excitability in heterozygous Scn8a-R1627H mutants.
The data support a model where ankyrinG (show ANK3 Antibodies)-binding is required for preferential Nav1.6 insertion into the axon initial segment plasma membrane during development.
the degenerating muscle mutation is a loss of function mutation of scn8a
N1768D mutation of SCN8A is sufficient to induce seizures and SUDEP in knock-in mice.
APP (show APP Antibodies) enhances Nav1.6 sodium channel cell surface expression through a Go-coupled JNK (show MAPK8 Antibodies) pathway
This study provided evidence for a direct link between sodium channel activity and modulation of Rac1 and ERK1/2 (show MAPK1/3 Antibodies) activation in ATP-stimulated microglia, possibly by regulating Ca(2 (show CA2 Antibodies)+) transients
results identify the hippocampus as an important structure in the mediation of Scn8a-dependent seizure protection and suggest that selective targeting of Scn8a activity might be efficacious in patients with epilepsy.
This gene encodes a member of the sodium channel alpha subunit gene family. The encoded protein forms the ion pore region of the voltage-gated sodium channel. This protein is essential for the rapid membrane depolarization that occurs during the formation of the action potential in excitable neurons. Mutations in this gene are associated with mental retardation, pancerebellar atrophy and ataxia. Alternate splicing results in multiple transcript variants.
hNa6/Scn8a voltage-gated sodium channel
, sodium channel protein type 8 subunit alpha
, voltage-gated sodium channel subunit alpha Nav1.6
, Na+ channel
, peripheral nerve protein type 4
, sodium channel 6
, sodium channel protein type VIII subunit alpha
, sodium channel voltage-gated type VIII alpha polypeptide
, sodium channel, voltage-gated, type 8, alpha polypeptide
, sodium channel, voltage-gated, type 8, alpha subunit
, sodium channel, voltage-gated, type VIII, alpha polypeptide
, ataxia 3