| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CLEC5A |
| Uniprot No | Q9NY25 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 28-188aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSPQIFNKSNDGFTTTRSYGTVSQIFGSS SPSPNGFITTRSYGTVCPKDWEFYQARCFFLSTSESSWNESRDFCKGKGS TLAIVNTPEKLKFLQDITDAEKYFIGLIYHREEKRWRWINNSVFNGNVTN QNQNFNCATIGLTKTFDAASCDISYRRICEKNAK |
| 预测分子量 | 21 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CLEC5A重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**：*CLEC5A is a critical receptor in innate immunity against dengue virus infection*
**作者**：Chen, S.T. 等人
**摘要**：该研究揭示了CLEC5A作为登革热病毒的关键识别受体，通过与病毒表面蛋白结合激活巨噬细胞，引发促炎细胞因子风暴。实验中使用CLEC5A重组蛋白及阻断性抗体证实其调控炎症反应的机制，为治疗登革热提供了潜在靶点。
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2. **文献名称**：*Structural basis of CLEC5A recognition by viral glycoproteins*
**作者**：Hsieh, H.P. 等人
**摘要**：通过X射线晶体学解析CLEC5A重组蛋白的配体结合域结构，研究发现其与日本脑炎病毒糖蛋白E的特异性相互作用。重组蛋白的功能实验揭示了CLEC5A在病原识别中的分子基础，为开发抑制过度炎症的抑制剂奠定结构基础。
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3. **文献名称**：*Targeting CLEC5A with soluble recombinant protein attenuates sepsis-induced inflammation*
**作者**：Lin, Y.L. 等人
**摘要**：研究构建了可溶性CLEC5A重组蛋白作为诱饵受体，在败血症小鼠模型中有效竞争性结合病原相关分子，抑制下游TLR2信号通路，显著降低促炎因子水平，证实其治疗脓毒症相关炎症的潜力。
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**备注**：上述文献为示例，实际引用时需核实具体作者及期刊信息。CLEC5A重组蛋白的研究多聚焦于其病原识别机制及作为治疗靶点的应用，涉及病毒感染、结构生物学及炎症性疾病模型。
CLEC5A (C-type lectin domain family 5 member A), also known as MDL-1. is a transmembrane protein belonging to the C-type lectin receptor (CLR) family. It is primarily expressed on myeloid cells, including macrophages, neutrophils, and dendritic cells, where it functions as a pattern recognition receptor (PRR). CLEC5A recognizes pathogen-associated molecular patterns (PAMPs) from viruses, bacteria, and fungi, such as dengue virus envelope protein, Staphylococcus aureus, and Aspergillus fumigatus. Its activation triggers pro-inflammatory signaling through association with the adaptor protein DAP12. leading to the release of cytokines (e.g., TNF-α, IL-6) and chemokines, which are critical for host defense but may also contribute to hyperinflammation in severe infections.
Recombinant CLEC5A protein, typically produced in mammalian or insect expression systems, includes the extracellular domain responsible for ligand binding. This engineered protein retains the ability to interact with pathogens or their components, making it a valuable tool for studying receptor-ligand interactions, immune signaling pathways, and inflammatory responses in vitro. Researchers utilize it to investigate mechanisms underlying diseases like dengue hemorrhagic fever, rheumatoid arthritis, and sepsis, where CLEC5A-mediated immune dysregulation plays a role. Additionally, recombinant CLEC5A is explored in therapeutic development, including blocking antibodies or decoy receptors to mitigate excessive inflammation without compromising microbial clearance. Its dual role in immunity and pathology underscores its significance as both a research target and a potential clinical intervention point.
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