Analytical Data
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基因名
ATP7b
- Application
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别名
PWD; WC1; WD; WND; Wilson Disease Protein; Copper pump 2; Wilson disease-associated protein
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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
P35670
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表达区间
Thr59~Val426
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分子量
43kDa
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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
ATP7B, a copper-transporting ATPase, plays a crucial role in maintaining copper homeostasis in the human body. Mutations in the ATP7B gene are associated with Wilson’s disease, a genetic disorder that leads to excessive copper accumulation, particularly in the liver and brain, resulting in hepatic and neurological symptoms. The study of recombinant ATP7B protein has gained significant attention due to its potential applications in understanding the mechanistic role of the protein in copper transport, as well as its implications in disease pathology. By producing ATP7B recombinantly, researchers can investigate the structure-function relationships, analyze the effects of specific mutations, and develop targeted therapies. Furthermore, the study of ATP7B can provide insights into copper metabolism disorders beyond Wilson’s disease, shedding light on the broader implications of copper dysregulation in various diseases. Given the complexity of copper transport and its critical biological functions, ATP7B serves as a key model for exploring therapeutic interventions aimed at restoring copper balance in affected patients.
