Analytical Data
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基因名
SCN1A
- Application
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别名
Sodium channel protein brain I subunit alpha;Sodium channel protein type I subunit alpha;Voltage-gated sodium channel subunit alpha Nav1.1
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种属
Human
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表达系统
E. coli
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标签
N- His
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纯度
Greater than 90% as determined by SDS-PAGE.
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蛋白编号
P35498
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表达区间
1-128aa
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分子量
18.5 kDa
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内毒素
< 1.0 EU per μg protein as determined by the LAL method.
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性状
Freeze-dried powder
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缓冲液
PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300.
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复溶方法
Reconstitute in ddH2O to a concentration of 0.1-0.5 mg/mL. Do not vortex.
- 个性化定制
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稳定性测试
The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37℃ for 48h, and no obvious degradation and precipitation were observed. The loss rate isless than 8% within the expiration date under appropriate storage condition.
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保存条件 & 期限
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
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运输条件
In general, recombinant proteins are supplied as lyophilized powder and shipped at ambient temperature. For bulk packages, the proteins are provided as frozen liquid and shipped with blue ice, unless otherwise requested by the customer.
Quality inspection process
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Protein Description
SCN1A encodes the alpha subunit of the voltage-gated sodium channel NaV1.1, which is crucial for the generation and propagation of action potentials in neurons. Mutations in the SCN1A gene are associated with various neurological disorders, particularly Dravet syndrome, a severe form of epilepsy that manifests in early childhood. Due to its significant role in neuronal excitability and synaptic transmission, SCN1A has garnered considerable attention in both clinical and research settings. Understanding the functional implications of SCN1A mutations requires detailed studies of the recombinant protein, which allows for the investigation of channel dynamics, pharmacological properties, and the effects of specific mutations. Furthermore, the development of SCN1A-recombinant protein not only enhances our understanding of its structure-function relationships but also aids in the identification of potential therapeutic targets for sodium channel dysfunction-related disorders. Insights gained from recombinant SCN1A can pave the way for innovative treatments, including the exploration of small molecules and gene therapies aimed at correcting or mitigating the effects of SCN1A mutations. Consequently, thorough research on SCN1A recombinant proteins is essential for unraveling the complexities of sodium channel biology and for advancing the management of epilepsy and related neurological disorders.
