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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MIP4a |
| Uniprot No | Q9Y258 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 24-94aa |
| 氨基酸序列 | TRGSDISKTC CFQYSHKPLP WTWVRSYEFT SNSCSQRAVI FTTKRGKKVC THPRKKWVQK YISLLKTPKQ L |
| 预测分子量 | 8.4 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. |
以下是基于学术文献常见主题模拟的MIP4a(可能与CCL18等趋化因子相关)重组蛋白研究示例。建议通过PubMed或Google Scholar核实具体文献：
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1. **文献名称**：*Expression and Functional Characterization of Recombinant MIP-4α/CCL18 in Inflammatory Disease Models*
**作者**：Chen L, et al.
**摘要**：研究报道了利用哺乳动物细胞系统成功表达重组MIP4a蛋白，并证实其在体外显著促进单核细胞迁移，且在类风湿性关节炎模型中加剧炎症反应，提示其作为治疗靶点的潜力。
2. **文献名称**：*Recombinant MIP4a Enhances Dendritic Cell Maturation and Antitumor Immunity*
**作者**：Kim S, et al.
**摘要**：通过真核表达系统制备功能性MIP4a，证明其可激活树突状细胞，增强肿瘤抗原呈递能力，在黑色素瘤小鼠模型中联合疫苗使用可显著延长生存期。
3. **文献名称**：*Structural Analysis of MIP4a Reveals Key Residues for Chemotactic Activity*
**作者**：Garcia-Ruiz E, et al.
**摘要**：采用X射线衍射解析重组MIP4a的三维结构，结合点突变实验确定其与受体CCR3结合的关键区域，为设计趋化因子抑制剂提供结构基础。
4. **文献名称**：*MIP4a Recombinant Protein Attenuates Pulmonary Fibrosis via Modulating Macrophage Phenotypes*
**作者**：Zhang R, et al.
**摘要**：研究显示，原核表达的重组MIP4a可通过调控肺组织巨噬细胞极化，减少胶原沉积，改善博来霉素诱导的小鼠肺纤维化病理进展。
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**注意**：以上为模拟示例，实际文献可能存在名称或内容差异。建议使用关键词“MIP4a recombinant protein”“CCL18 recombinant”或结合疾病名称(如癌症、纤维化)在学术数据库中检索确切文献。
MIP-4a (Macrophage Inflammatory Protein-4 Alpha), also known as CCL18. is a chemokine belonging to the CC subfamily. It is primarily secreted by antigen-presenting cells, such as dendritic cells and macrophages, under inflammatory or immunomodulatory conditions. Structurally, it consists of a conserved N-terminal region and a characteristic CC motif that facilitates interactions with specific G protein-coupled receptors, notably CCR8. MIP-4a plays a pivotal role in directing immune cell migration, particularly influencing T lymphocytes, immature dendritic cells, and regulatory T cells (Tregs), thereby modulating adaptive immunity and maintaining immune tolerance.
Research highlights its dual role in both promoting and suppressing disease progression. In cancer, MIP-4a is often upregulated in tumor-associated macrophages and correlates with poor prognosis in malignancies like breast and ovarian cancers. It fosters an immunosuppressive tumor microenvironment by recruiting Tregs and inhibiting cytotoxic T-cell activity. Conversely, in autoimmune disorders such as rheumatoid arthritis, elevated MIP-4a levels contribute to chronic inflammation by enhancing leukocyte infiltration.
Recombinant MIP-4a is produced via heterologous expression systems (e.g., E. coli or mammalian cells), ensuring high purity and bioactivity for experimental use. Its applications span in vitro chemotaxis assays, immune cell differentiation studies, and preclinical models evaluating therapeutic targeting of chemokine pathways. Recent drug development efforts focus on neutralizing antibodies or small-molecule inhibitors against MIP-4a/CCR8 axis to counteract immune evasion in cancers or mitigate inflammatory damage in autoimmune diseases. Despite progress, its context-dependent functions warrant further exploration to optimize clinical translation.
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