SCN1A sirna

SCN1A siRNA (Rat)

Cat. Num. AAA8231456

• Reactivity: Rat
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: SCN1A; SCN1A siRNA (Rat); Sodium channel protein type 1 subunit alpha; Sodium channel protein brain I subunit alpha; Sodium channel protein type I subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.1; SCN1A sirna

• Host: Synthetic
• Reactivity: Rat
• Specificity: SCN1A siRNA (Rat) 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: 2009

• Applicable Applications for SCN1A 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 rat SCN1A 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 SCN1A sirna

siRNA to inhibit SCN1A expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 13540709
• NCBI GeneID: 81574
• NCBI Accession #: NP_110502.1
• NCBI GenBank Nucleotide #: NM_030875.1
• UniProt Accession #: P04774
• Molecular Weight: 228,770 Da
• NCBI Official Full Name: sodium channel protein type 1 subunit alpha
• NCBI Official Synonym Full Names: sodium channel, voltage-gated, type I, alpha subunit
• NCBI Official Symbol: Scn1a
• NCBI Protein Information: sodium channel protein type 1 subunit alpha
• UniProt Protein Name: Sodium channel protein type 1 subunit alpha
• Protein Family: Sodium channel protein
• UniProt Gene Name: Scn1a
• UniProt Entry Name: SCN1A_RAT

NCBI Description

has voltage gated sodium ion channel activity; plays a role in generation of action potential [RGD, Feb 2006]

Uniprot Description

SCN1A: 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. Defects in SCN1A are the cause of generalized epilepsy with febrile seizures plus type 2 (GEFS+2). Generalized epilepsy with febrile seizures-plus refers to a rare autosomal dominant, familial condition with incomplete penetrance and large intrafamilial variability. Patients display febrile seizures persisting sometimes beyond the age of 6 years and/or a variety of afebrile seizure types. GEFS+ is a disease combining febrile seizures, generalized seizures often precipitated by fever at age 6 years or more, and partial seizures, with a variable degree of severity. Defects in SCN1A are a cause of severe myoclonic epilepsy in infancy (SMEI); also called Dravet syndrome. SMEI is a rare disorder characterized by generalized tonic, clonic, and tonic-clonic seizures that are initially induced by fever and begin during the first year of life. Later, patients also manifest other seizure types, including absence, myoclonic, and simple and complex partial seizures. Psychomotor development delay is observed around the second year of life. SMEI is considered to be the most severe phenotype within the spectrum of generalized epilepsies with febrile seizures-plus. Defects in SCN1A are a cause of intractable childhood epilepsy with generalized tonic-clonic seizures (ICEGTC). ICEGTC is a disorder characterized by generalized tonic-clonic seizures beginning usually in infancy and induced by fever. Seizures are associated with subsequent mental decline, as well as ataxia or hypotonia. ICEGTC is similar to SMEI, except for the absence of myoclonic seizures. Defects in SCN1A are the cause of familial hemiplegic migraine type 3 (FHM3). FHM3 is an autosomal dominant severe subtype of migraine with aura characterized by some degree of hemiparesis during the attacks. The episodes are associated with variable features of nausea, vomiting, photophobia, and phonophobia. Age at onset ranges from 6 to 15 years. FHM is occasionally associated with other neurologic symptoms such as cerebellar ataxia or epileptic seizures. A unique eye phenotype of elicited repetitive daily blindness has also been reported to be cosegregating with FHM in a single Swiss family. Defects in SCN1A are the cause of familial febrile convulsions type 3A (FEB3A); also known as familial febrile seizures 3. Febrile convulsions are seizures associated with febrile episodes in childhood without any evidence of intracranial infection or defined pathologic or traumatic cause. It is a common condition, affecting 2-5% of children aged 3 months to 5 years. The majority are simple febrile seizures (generally defined as generalized onset, single seizures with a duration of less than 30 minutes). Complex febrile seizures are characterized by focal onset, duration greater than 30 minutes, and/or more than one seizure in a 24 hour period. The likelihood of developing epilepsy following simple febrile seizures is low. Complex febrile seizures are associated with a moderately increased incidence of epilepsy. Belongs to the sodium channel (TC 1.A.1.10) family. Nav1.1/SCN1A subfamily. 2 isoforms of the human protein are produced by alternative splicing.

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

Cellular Component: voltage-gated sodium channel complex; membrane; cell soma; axon; T-tubule; plasma membrane; Z disc

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

Biological Process: regulation of action potential; neuromuscular process controlling posture; regulation of membrane potential; sodium ion transport; action potential propagation; generation of action potential; adult walking behavior