纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | LILRB4 |
Uniprot No | Q8NHJ6 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 17-257aa |
氨基酸序列 | PRTH MQAGPLPKPT LWAEPGSVIS WGNSVTIWCQ GTLEAREYRL DKEESPAPWD RQNPLEPKNK ARFSIPSMTE DYAGRYRCYY RSPVGWSQPS DPLELVMTGA YSKPTLSALP SPLVTSGKSV TLLCQSRSPM DTFLLIKERA AHPLLHLRSE HGAQQHQAEF PMSPVTSVHG GTYRCFSSHG FSHYLLSHPS DPLELIVSGS LEDPRPSPTR SVSTAAGPED QPLMPTGSVP HSGLRRHWEV LIGVLVVSIL LLSLLLFLLL QHWRQGKHRT LAQRQADFQR PPGAAEPEPK DGGLQRRSSP AADVQGENFC AAVKNTQPED GVEMDTRQSP HDEDPQA |
预测分子量 | 31 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LILRB4重组蛋白的3篇参考文献示例(基于领域内研究方向的模拟概括,非真实文献):
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1. **文献名称**: *Structural basis of LILRB4-mediated immune evasion in acute myeloid leukemia*
**作者**: Chen et al.
**摘要**: 本研究解析了LILRB4重组蛋白的晶体结构,发现其通过结合肿瘤微环境中的特定配体(如ANGPTLs)激活SHP-1/2信号通路,抑制T细胞活性,促进AML(急性髓系白血病)的免疫逃逸。重组LILRB4蛋白的体外实验验证了其免疫检查点功能。
2. **文献名称**: *LILRB4 recombinant protein as a potential therapeutic target for autoimmune diseases*
**作者**: Smith et al.
**摘要**: 通过表达并纯化LILRB4重组蛋白,研究发现其可抑制单核细胞炎症因子的释放,并调节树突状细胞的抗原呈递功能,提示靶向LILRB4可能通过重组蛋白或抗体干预治疗类风湿性关节炎等自身免疫疾病。
3. **文献名称**: *LILRB4 interacts with extracellular matrix components via its immunoglobulin domains*
**作者**: Wang et al.
**摘要**: 利用重组LILRB4蛋白进行体外结合实验,发现其胞外段特异性结合胶原蛋白和层粘连蛋白,揭示了LILRB4在肿瘤转移中可能通过调节细胞-基质黏附促进恶性细胞浸润的分子机制。
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**注**:以上为模拟概括,实际文献需通过PubMed/Google Scholar检索关键词“LILRB4 recombinant protein”“LILRB4 structure/function”获取。近期研究多聚焦于LILRB4在肿瘤免疫治疗中的应用潜力。
LILRB4 (leukocyte immunoglobulin-like receptor B4), also known as ILT3 or CD85k, is an inhibitory immune checkpoint protein belonging to the leukocyte immunoglobulin-like receptor (LIR/LILR) family. It is primarily expressed on myeloid-derived suppressor cells (MDSCs), dendritic cells, and certain subsets of monocytes/macrophages. Structurally, LILRB4 contains immunoglobulin-like extracellular domains and cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIMs) that mediate immunosuppressive signaling.
Functionally, LILRB4 interacts with MHC class I molecules and other ligands to downregulate immune responses, maintaining peripheral tolerance and preventing excessive inflammation. In pathological contexts, particularly cancer, LILRB4 overexpression is associated with immune evasion. It suppresses T-cell activity, promotes an immunosuppressive tumor microenvironment, and facilitates tumor progression. Notably, LILRB4 has been identified as a key regulator in acute myeloid leukemia (AML), where it supports leukemia stem cell survival and bone marrow infiltration.
Recombinant LILRB4 proteins are engineered through mammalian expression systems (e.g., CHO or HEK293 cells) to preserve native post-translational modifications and ligand-binding capabilities. These proteins typically include the extracellular domain (ECD) with Fc fusion tags for enhanced stability. Applications include: 1) Basic research to decipher LILRB4-mediated signaling pathways; 2) Therapeutic antibody screening for cancer immunotherapy; 3) Diagnostic biomarker development for myeloid malignancies; 4) Structural studies using techniques like X-ray crystallography.
Recent studies highlight LILRB4 as a promising therapeutic target. Antibodies blocking LILRB4 have shown potential in restoring anti-tumor immunity in preclinical models. The recombinant protein serves as a critical tool for validating drug candidates and understanding immune tolerance mechanisms in oncology and autoimmune diseases.
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