关键信息
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基因名
Arylsulfatase A/ARSA
- 应用
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别名
MLD; ASA; Metachromatic Leucodystrophy; Cerebroside-sulfatase
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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
P15289
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表达区间
Arg19~Gly293
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分子量
33kDa
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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.
质检流程
相关产品
背景信息
Arylsulfatase A (ARSA) is a crucial enzyme involved in the catabolism of sulfated glycosaminoglycans and is primarily expressed in the lysosomes. Deficiency of ARSA leads to a rare genetic disorder known as Metachromatic Leukodystrophy (MLD), characterized by the accumulation of sulfated lipids, demyelination, and neurodegeneration. Given the severe neurological implications of ARSA deficiency, there has been a significant focus on developing therapeutic strategies, including enzyme replacement therapy (ERT). The recombinant production of ARSA has become a central aspect of these efforts. Understanding the structure-function relationships of ARSA, optimizing its production in various expression systems, and enhancing its stability and delivery are vital for developing effective treatment options for MLD patients. Recent advancements in recombinant DNA technology have enabled the generation of functional and commercially viable ARSA proteins, paving the way for clinical applications. Furthermore, the exploration of potential gene therapy approaches and small molecule pharmacological chaperones is also underway to correct the underlying genetic defects associated with ARSA deficiency. As research continues to unfold, the dual focus on the biochemical characterization of ARSA and the evaluation of innovative therapeutic modalities represents a promising frontier in the battle against MLD and related lysosomal storage disorders.
