| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SLAMF8 |
| Uniprot No | Q9P0V8 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-285aa |
| 氨基酸序列 | MVMRPLWSLLLWEALLPITVTGAQVLSKVGGSVLLVAARPPGFQVREAIWRSLWPSEELLATFFRGSLETLYHSRFLGRAQLHSNLSLELGPLESGDSGNFSVLMVDTRGQPWTQTLQLKVYDAVPRPVVQVFIAVERDAQPSKTCQVFLSCWAPNISEITYSWRRETTMDFGMEPHSLFTDGQVLSISLGPGDRDVAYSCIVSNPVSWDLATVTPWDSCHHEAAPGKASYKDVLLVVVPVSLLLMLVTLFSAWHWCPCSGKKKKDVHADRVGPETENPLVQDLP |
| 预测分子量 | 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SLAMF8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**：*SLAMF8 regulates inflammatory response in macrophages via modulating TLR/NF-κB signaling*
**作者**：Li X, et al.
**摘要**：本研究利用重组SLAMF8蛋白探究其在巨噬细胞炎症反应中的作用，发现SLAMF8通过抑制TLR4/NF-κB通路减轻脂多糖诱导的炎症因子释放，提示其可能作为炎症性疾病的潜在治疗靶点。
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2. **文献名称**：*Expression and functional characterization of recombinant human SLAMF8 in autoimmune disease models*
**作者**：Zhang Y, et al.
**摘要**：该研究成功在大肠杆菌中表达并纯化重组人源SLAMF8蛋白，实验表明其可抑制T细胞过度活化，并在类风湿性关节炎小鼠模型中减少关节炎症，证实其免疫调节功能。
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3. **文献名称**：*Structural insights into SLAMF8-mediated immune regulation through crystallographic analysis*
**作者**：Kumar S, et al.
**摘要**：通过X射线晶体学解析了重组SLAMF8蛋白的分子结构，揭示了其与配体CD48结合的关键位点，为设计靶向SLAMF8的免疫治疗药物提供了结构基础。
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**注**：以上文献信息为示例性概括，实际引用需以真实发表的论文为准。若需具体文献，建议通过PubMed或Web of Science以关键词“SLAMF8 recombinant protein”检索。
SLAMF8 (Signaling Lymphocytic Activation Molecule Family Member 8), also known as CD352 or BLAME, is a cell surface receptor belonging to the SLAM family of immune-regulatory proteins. These receptors are primarily expressed on hematopoietic cells, including natural killer (NK) cells, T cells, dendritic cells, and macrophages. Structurally, SLAMF8 features an extracellular region with immunoglobulin-like domains, a transmembrane region, and a cytoplasmic tail containing immunoreceptor tyrosine-based switch motifs (ITSMs). These motifs enable interactions with adaptor proteins like SAP (SLAM-associated protein), which mediate downstream signaling pathways involved in immune cell activation, differentiation, and effector functions.
SLAMF8 plays a dual role in modulating immune responses. It can either enhance or inhibit cellular activity depending on context, ligand engagement, and interacting partners. Studies suggest its involvement in regulating NK cell cytotoxicity, T cell exhaustion, and macrophage polarization. In pathological conditions, SLAMF8 is implicated in chronic inflammation, autoimmune disorders, and cancer. For example, elevated SLAMF8 expression in tumor-associated macrophages correlates with immunosuppressive microenvironments, potentially promoting tumor immune evasion.
Recombinant SLAMF8 proteins are engineered to study its biological functions and therapeutic potential. These proteins typically include the extracellular domain produced in mammalian expression systems to ensure proper folding and post-translational modifications. Researchers use them to investigate ligand-receptor interactions, screen therapeutic antibodies, or develop decoy receptors to modulate immune signaling. Recent interest in SLAMF8 has grown due to its emerging role as a checkpoint regulator, with preclinical studies exploring its targeting for cancer immunotherapy or treatment of autoimmune diseases. However, its precise mechanisms and clinical relevance remain under active investigation.
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