Analytical Data
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基因名
SLC26A4-VLPs
- Application
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别名
(Sodium-independent chloride/iodide transporter)(Solute carrier family 26 member 4)
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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
O43511
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表达区间
1-780aa(H723R)
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分子量
86.7 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
SLC26A4, also known as the Pendred syndrome gene, encodes a protein involved in the transport of anions, such as chloride and iodide, across cell membranes. Mutations in this gene are associated with various disorders, including Pendred syndrome and enlarged vestibular aqueducts, which can lead to hearing loss and thyroid dysfunction. Researchers have turned to recombinant proteins and virus-like particles (VLPs) to better understand the structure and function of SLC26A4. By expressing this protein in a controlled system and assembling it into VLPs, scientists aim to investigate its interactions and physiological roles more effectively. The unique properties of VLPs allow for detailed biophysical studies, immunogenicity assessments, and potential vaccine development. This approach not only enhances our understanding of SLC26A4's mechanism but also paves the way for innovative therapeutic strategies targeting associated pathologies, thereby addressing a critical gap in the current understanding of genetic hearing loss and thyroid disorders linked to SLC26A4 mutations.












