SCN8A sirna

SCN8A siRNA (Human)

Cat. Num. AAA8240601

• Gene Names: SCN8A; MED; PN4; CIAT; NaCh6; CERIII; EIEE13; Nav1.6
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: SCN8A; SCN8A siRNA (Human); MED; Sodium channel protein type 8 subunit alpha; Sodium channel protein type VIII subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.6; SCN8A sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: SCN8A siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 1939

• Applicable Applications for SCN8A sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human SCN8A gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for SCN8A sirna

siRNA to inhibit SCN8A expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 295789135
• NCBI GeneID: 6334
• NCBI Accession #: NP_001171455.1
• NCBI GenBank Nucleotide #: NM_001177984.2
• UniProt Accession #: Q9UQD0; O95788; Q9NYX2; Q9UPB2; B9VWG8
• Molecular Weight: 220,798 Da
• NCBI Official Full Name: sodium channel protein type 8 subunit alpha isoform 2
• NCBI Official Synonym Full Names: sodium channel, voltage gated, type VIII alpha subunit
• NCBI Official Symbol: SCN8A
• NCBI Official Synonym Symbols: MED; PN4; CIAT; NaCh6; CERIII; EIEE13; Nav1.6
• NCBI Protein Information: sodium channel protein type 8 subunit alpha
• UniProt Protein Name: Sodium channel protein type 8 subunit alpha
• Protein Family: Sodium channel protein
• UniProt Gene Name: SCN8A
• UniProt Synonym Gene Names: MED
• UniProt Entry Name: SCN8A_HUMAN

NCBI Description

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.[provided by RefSeq, May 2010]

Uniprot Description

SCN8A: Mediates the voltage-dependent sodium ion permeability of excitable membranes. Assuming opened or closed conformations in response to the voltage difference across the membrane, the protein forms a sodium-selective channel through which Na(+) ions may pass in accordance with their electrochemical gradient. In macrophages and melanoma cells, isoform 5 may participate in the control of podosome and invadopodia formation. Defects in SCN8A are the cause of cognitive impairment with or without cerebellar ataxia (CIAT). A disorder characterized by markedly delayed cognitive and motor development, attention deficit disorder, and cerebellar ataxia. Features include bilateral esophoria, strabismatic amblyopia, unsustained gaze evoked nystagmus on horizontal gaze, ataxic gait, dysmetria in the upper limbs and dysarthria, with normal strength, tone, and reflexes. Defects in SCN8A are the cause of epileptic encephalopathy, early infantile, type 13 (EIEE13). A form of epilepsy characterized by frequent tonic seizures or spasms beginning in infancy with a specific EEG finding of suppression-burst patterns, characterized by high-voltage bursts alternating with almost flat suppression phases. Patients may progress to West syndrome, which is characterized by tonic spasms with clustering, arrest of psychomotor development, and hypsarrhythmia on EEG. EIEE13 is a severe form consisting of early-onset seizures, features of autism, intellectual disability, ataxia, and sudden unexplained death in epilepsy. Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.6/SCN8A subfamily. 5 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, multi-pass; Membrane protein, integral; Channel, sodium

Chromosomal Location of Human Ortholog: 12q13

Cellular Component: voltage-gated sodium channel complex; cell soma; cytoplasmic membrane-bound vesicle; dendrite; integral to membrane; plasma membrane; Z disc

Molecular Function: voltage-gated sodium channel activity; ATP binding

Biological Process: myelination; nervous system development; muscle development; sensory perception of sound; response to toxin; neuromuscular process; sodium ion transport; generation of action potential; adult walking behavior; peripheral nervous system development

Disease: Epileptic Encephalopathy, Early Infantile, 13; Cognitive Impairment With Or Without Cerebellar Ataxia