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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TL1A |
| Uniprot No | O95150 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 93-251aa |
| 氨基酸序列 | DKPRAHLTVVRQTPTQHFKNQFPALHWEHELGLAFTKNRMNYTNKFLLIP ESGDYFIYSQVTFRGMTSECSEIRQAGRPNKPDSITVVITKVTDSYPEPT QLLMGTKSVCEVGSNWFQPIYLGAMFSLQEGDKLMVNVSDISLVDYTKED KTFFGAFLL |
| 预测分子量 | 20 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TL1A重组蛋白的3篇代表性文献，简要总结如下：
1. **文献名称**：*TL1A is a TNF-like ligand for DR3 and regulates T cell activation*
**作者**：Migone, T.S. 等(2002)
**摘要**：首次克隆并鉴定TL1A为TNF超家族成员，发现其通过结合死亡受体DR3激活NF-κB信号通路，促进T细胞活化和细胞因子分泌，为炎症性疾病研究奠定基础。
2. **文献名称**：*TL1A modulates intestinal inflammation and fibrosis in experimental colitis*
**作者**：Papi, F. 等(2012)
**摘要**：利用重组TL1A蛋白处理小鼠结肠炎模型，证明TL1A通过增强Th1/Th17免疫反应和成纤维细胞活化，加剧肠道炎症和纤维化，提示其在IBD中的潜在治疗靶点。
3. **文献名称**：*Recombinant TL1A synergizes with IL-12/IL-18 to enhance NK cell cytotoxicity and IFN-γ production*
**作者**：Zhan, Y. 等(2016)
**摘要**：研究重组TL1A蛋白与IL-12/IL-18的协同作用，发现其通过激活AKT/mTOR通路显著增强NK细胞抗肿瘤活性，为癌症免疫治疗提供新策略。
4. **文献名称**：*Structural and functional characterization of TL1A-DR3 interaction*
**作者**：Shih, D.Q. 等(2008)
**摘要**：解析重组TL1A蛋白与DR3受体复合物的晶体结构，揭示其结合界面关键氨基酸残基，为靶向TL1A/DR3通路的药物设计提供结构依据。
以上研究涵盖TL1A的分子机制、疾病关联及治疗应用方向。
TL1A (Tumor Necrosis Factor Ligand Superfamily Member 15. TNFSF15) is a cytokine belonging to the tumor necrosis factor (TNF) superfamily, primarily involved in regulating inflammatory and immune responses. It was first identified in 2002 as an endothelial cell-derived protein capable of activating T cells and inducing IFN-γ production. Structurally, TL1A exists as a type II transmembrane protein that can be proteolytically cleaved to release a soluble cytokine form. Its functional receptor, Death Receptor 3 (DR3/TNFRSF25), is expressed on lymphocytes including Th1. Th17. and innate lymphoid cells, while a decoy receptor (DcR3) modulates its signaling.
TL1A-DR3 interaction triggers NF-κB and MAPK signaling pathways, promoting pro-inflammatory cytokine production (e.g., IL-2. IL-13) and enhancing T cell activation/differentiation. This axis plays critical roles in mucosal immunity and pathological inflammation, with strong associations to inflammatory bowel disease (IBD), rheumatoid arthritis, psoriasis, and celiac disease. Genetic studies link TNFSF15 polymorphisms to IBD susceptibility across ethnic populations.
Recombinant TL1A protein, typically produced in mammalian expression systems, retains the receptor-binding extracellular domain (amino acids 72-251). It serves as a vital tool for studying TL1A-mediated immune mechanisms and validating therapeutic candidates. Recent drug development focuses on neutralizing TL1A or DR3 through monoclonal antibodies to suppress chronic inflammation, with several candidates in clinical trials for IBD and fibrotic diseases. Conversely, recombinant TL1A has been explored for enhancing anti-tumor immunity by activating effector T cells. Despite therapeutic potential, its dual roles in immune activation and regulation require careful contextual evaluation in disease models.
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