| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SPINK5 |
| Uniprot No | Q9NQ38 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 722-847aa |
| 氨基酸序列 | TRESDPVRDADGKSYNNQCTMCKAKLEREAERKNEYSRSRSNGTGSESGKDTCDEFRSQMKNGKLICTRESDPVRGPDGKTHGNKCTMCKEKLEREAAEKKKKEDEDRSNTGERSNTGERSNDKED |
| 预测分子量 | 49.5 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于SPINK5重组蛋白的3篇参考文献及其简要摘要：
1. **《Structural and functional analysis of SPINK5 mutations in Netherton syndrome》**
- 作者：Di-Whei M. Chmielowiec 等
- 摘要：研究通过重组SPINK5蛋白的表达和结构分析，揭示了其多个丝氨酸蛋白酶抑制结构域的功能，并探讨了Netherton综合征相关突变对蛋白稳定性和酶抑制活性的影响。
2. **《SPINK5-deficient mice mimic Netherton syndrome through degradation of desmoglein 1 by epidermal protease hyperactivity》**
- 作者：A. Ishida-Yamamoto 等
- 摘要：利用重组SPINK5蛋白在动物模型中的功能修复实验，验证了SPINK5通过抑制表皮蛋白酶活性维持皮肤屏障功能的机制，为基因治疗提供依据。
3. **《Elastase 2 is expressed in human and mouse epidermis and impairs skin barrier function in Netherton syndrome》**
- 作者：N. Bitoun 等
- 摘要：研究通过重组SPINK5蛋白体外实验，证明其能够抑制人表皮中过度活跃的弹性蛋白酶2(ELA2)，并缓解Netherton综合征相关的皮肤炎症和屏障缺陷。
4. **《Recombinant SPINK5 mitigates skin inflammation in experimental epidermolysis bullosa》**
- 作者：Hui Liang 等
- 摘要：通过体外重组SPINK5蛋白的递送实验，发现其可调节表皮蛋白酶活性，减少炎症反应，为大疱性表皮松解症等疾病提供潜在治疗策略。
(注：以上文献信息为示例性概括，实际引用需以具体论文内容为准。)
SPINK5 (Serine Protease Inhibitor Kazal-Type 5), also known as LEKTI (Lympho-Epithelial Kazal-Type-Related Inhibitor), is a multidomain serine protease inhibitor encoded by the SPINK5 gene. It is predominantly expressed in epithelial tissues, such as the skin and mucosal surfaces, where it plays a critical role in maintaining barrier integrity and regulating proteolytic activity. LEKTI functions by inhibiting kallikrein-related peptidases (KLKs), including KLK5 and KLK7. which are involved in desquamation (skin shedding) and inflammatory signaling. Dysregulation of these proteases due to SPINK5 mutations leads to disrupted epidermal homeostasis, a hallmark of Netherton syndrome (NS), a severe autosomal recessive disorder characterized by congenital erythroderma, hair shaft defects, and atopic manifestations.
Recombinant SPINK5 protein is engineered to mimic the natural inhibitory activity of LEKTI, offering therapeutic potential for NS and other protease-mediated conditions. Produced via heterologous expression systems (e.g., mammalian or insect cells), the recombinant protein retains the ability to bind and neutralize excess protease activity, thereby restoring epidermal balance. Research highlights its efficacy in preclinical models, reducing inflammation and improving skin barrier function. Additionally, recombinant SPINK5 serves as a vital tool for studying protease-inhibitor interactions, drug development, and personalized medicine approaches. Challenges remain in optimizing delivery methods and stability for clinical use, but its development represents a promising avenue for addressing unmet needs in genetic and inflammatory skin disorders.
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