| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PDCD1LG2 |
| Uniprot No | Q9BQ51 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 20-220aa |
| 氨基酸序列 | LFTVTVPKELYIIEHGSNVTLECNFDTGSHVNLGAITASLQKVENDTSPH RERATLLEEQLPLGKASFHIPQVQVRDEGQYQCIIIYGVAWDYKYLTLKV KASYRKINTHILKVPETDEVELTCQATGYPLAEVSWPNVSVPANTSHSRT PEGLYQVTSVLRLKPPPGRNFSCVFWNTHVRELTLASIDLQSQMEPRTHP T |
| 预测分子量 | 23 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PDCD1LG2(PD-L2)重组蛋白的模拟参考文献示例，基于相关领域研究的典型方向整理：
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1. **文献名称**：**"Recombinant PDCD1LG2 Protein Production and Functional Characterization in Immune Regulation"**
**作者**：Chen X, Wang Y, et al.
**摘要**：本研究利用哺乳动物表达系统成功表达并纯化了PDCD1LG2(PD-L2)重组蛋白，验证其与受体PD-1的结合活性。体外实验表明，该重组蛋白可显著抑制T细胞增殖及细胞因子分泌，提示其在免疫检查点通路中的调控作用，为后续抗体药物开发提供基础。
2. **文献名称**：**"Structural Insights into PDCD1LG2-PD-1 Interaction by Cryo-EM Analysis of Recombinant Complex"**
**作者**：Tanaka K, Nakamura S, et al.
**摘要**：通过冷冻电镜技术解析PDCD1LG2重组蛋白与PD-1的复合物三维结构，揭示两者结合的关键表位及构象变化。研究为设计靶向PD-1/PD-L2通路的小分子抑制剂提供了结构生物学依据。
3. **文献名称**：**"Comparative Functional Analysis of PD-L1 and PD-L2 Recombinant Proteins in Tumor Immune Evasion"**
**作者**：Zhang L, Li H, et al.
**摘要**：对比PD-L1和PD-L2重组蛋白在肿瘤微环境中的功能差异，发现PD-L2重组蛋白对PD-1的结合亲和力低于PD-L1.但在特定肿瘤模型中仍能通过抑制T细胞活性促进免疫逃逸，提示其作为联合治疗靶点的潜力。
4. **文献名称**：**"Expression and Optimization of PDCD1LG2 in Escherichia coli for Antigen-Specific Antibody Screening"**
**作者**：Gupta R, Patel A, et al.
**摘要**：优化PDCD1LG2重组蛋白在原核系统中的可溶性表达，并通过体外筛选获得高亲和力单克隆抗体。该研究为基于PD-L2的免疫诊断试剂开发提供了高效制备方案。
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**注**：以上文献为模拟示例，实际文献需通过PubMed、Web of Science等数据库检索确认。建议使用关键词“PDCD1LG2 recombinant”“PD-L2 protein function”等查找最新研究。
PDCD1LG2 (Programmed Cell Death 1 Ligand 2), also known as PD-L2. is a transmembrane protein belonging to the B7 family of immune checkpoint regulators. It serves as a ligand for the PD-1 receptor (Programmed Cell Death Protein 1), a key inhibitory receptor expressed on activated T cells, B cells, and myeloid cells. PDCD1LG2 shares structural homology with PD-L1 (PDCD1LG1), including an immunoglobulin variable (IgV)-like domain and an immunoglobulin constant (IgC)-like domain, but exhibits distinct expression patterns and binding affinities. While PD-L1 is broadly expressed on both immune and non-immune cells, PD-L2 expression is more restricted, primarily observed on antigen-presenting cells (e.g., dendritic cells, macrophages) and certain tumor cells.
The PD-1/PD-L2 interaction plays a critical role in modulating T-cell activation and tolerance, helping to dampen immune responses and prevent autoimmunity. However, tumors often exploit this pathway by overexpressing PD-L2 to evade immune surveillance. Recombinant PDCD1LG2 proteins, typically produced in mammalian expression systems to ensure proper glycosylation and folding, are widely used in research to study immune checkpoint mechanisms, screen therapeutic antibodies, or evaluate PD-1 binding kinetics. These proteins retain the extracellular domain required for receptor interaction, enabling in vitro functional studies without membrane-associated complexities.
Therapeutic targeting of PD-L2 has gained interest due to its potential redundancy with PD-L1 in immune evasion and its association with resistance to anti-PD-1/PD-L1 therapies. Recombinant PDCD1LG2 tools contribute to developing next-generation immunotherapies, such as dual checkpoint inhibitors or bispecific antibodies, aiming to overcome limitations of current cancer treatments. Its role in autoimmune and infectious diseases also makes it a focus for balancing immune activation and suppression.
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