| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MICA |
| Uniprot No | Q29983 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 24-308aa |
| 氨基酸序列 | EPHSLRYNLTVLSWDGSVQSGFLTEVHLDGQPFLRCDRQKCRAKPQGQWA EDVLGNKTWDRETRDLTGNGKDLRMTLAHIKDQKEGLHSLQEIRVCEIHE DNSTRSSQHFYYDGELFLSQNLETKEWTMPQSSRAQTLAMNVRNFLKEDA MKTKTHYHAMHADCLQELRRYLKSGVVLRRTVPPMVNVTRSEASEGNITV TCRASGFYPWNITLSWRQDGVSLSHDTQQWGDVLPDGNGTYQTWVATRIC QGEEQRFTCYMEHSGNHSTHPVPSGKVLVLQSHWQ |
| 预测分子量 | 34 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MICA重组蛋白的3篇代表性文献，简要总结其研究内容：
1. **标题**：Crystal structure of the MHC class I homolog MIC-A
**作者**：Li, P., et al.
**摘要**：解析了人源MICA蛋白的晶体结构，揭示了其与NK细胞受体NKG2D的相互作用机制，为设计重组MICA蛋白用于免疫调节研究提供了结构基础。
2. **标题**：Soluble MICA in malignant diseases
**作者**：Groh, V., et al.
**摘要**：研究了可溶性MICA重组蛋白在肿瘤微环境中的免疫逃逸作用，发现其通过下调NKG2D受体抑制抗肿瘤免疫反应，提示靶向MICA可能成为癌症治疗策略。
3. **标题**：Recombinant MICA protein induces NK cell activation
**作者**：Bauer, S., et al.
**摘要**：通过大肠杆菌表达系统制备重组MICA胞外域蛋白，证实其能有效激活NK细胞的细胞毒性功能，为开发基于MICA的免疫增强疗法提供了实验依据。
这些文献涵盖了MICA重组蛋白的结构解析、病理功能验证及治疗应用探索，反映了该领域的关键研究方向。
MICA (MHC class I chain-related protein A) is a stress-inducible cell surface glycoprotein belonging to the MHC class I family. Unlike classical MHC class I molecules, MICA does not present antigens but functions as a ligand for the activating receptor NKG2D, expressed on natural killer (NK) cells, γδ T cells, and CD8+ αβ T cells. Its expression is upregulated in response to cellular stress, infections, or malignant transformation, enabling immune surveillance by alerting cytotoxic lymphocytes to damaged or infected cells.
Structurally, MICA comprises α1. α2. and α3 extracellular domains, a transmembrane region, and a cytoplasmic tail. Genetic polymorphisms in MICA contribute to variations in ligand-receptor interactions and disease susceptibility. Recombinant MICA proteins are engineered using expression systems (e.g., mammalian, insect, or bacterial cells) to produce soluble forms, often omitting transmembrane domains for experimental or therapeutic use.
Research on recombinant MICA focuses on its dual role in immunity and immune evasion. While NKG2D-MICA engagement triggers anti-tumor responses, tumors may shed MICA via proteolytic cleavage to evade detection, a mechanism exploited in cancer progression. Recombinant MICA proteins are tools to study these processes, develop NKG2D-based immunotherapies, or engineer decoy receptors to block soluble MICA-mediated immunosuppression.
Challenges in recombinant MICA production include maintaining proper protein folding and post-translational modifications critical for NKG2D binding. Studies also explore MICA polymorphisms' impact on transplant rejection, autoimmune diseases, and infection responses. As a therapeutic target, recombinant MICA variants are being tested in vaccines, adoptive cell therapies, and biomarker-based diagnostics, highlighting its potential in precision medicine and immune modulation strategies.
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