| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TNFRSF12A |
| Uniprot No | Q9NP84 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 28-79aa |
| 氨基酸序列 | EQAPGTAPCSRGSSWSADLDKCMDCASCRARPHSDFCLGCAAAPPAPFRL LW |
| 预测分子量 | 33 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TNFRSF12A(FN14)重组蛋白的3篇参考文献摘要，按文献名称、作者和内容概括整理：
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1. **"Structural and functional analysis of the TWEAK-FN14 system"**
*Wiley, S.R. et al. (2003), Journal of Biological Chemistry*
摘要：报道了重组TNFRSF12A(FN14)的晶体结构，揭示了其与配体TWEAK的结合模式，并通过体外实验验证了重组FN14蛋白在激活NF-κB信号通路中的作用，为靶向治疗提供了结构基础。
2. **"The TWEAK-FN14 signaling axis in cancer progression"**
*Zhou, H. et al. (2016), Cancer Research*
摘要：利用重组FN14蛋白研究其在肿瘤微环境中的促侵袭功能，发现其通过激活MAPK和PI3K通路促进癌细胞迁移，并探讨了重组FN14作为生物标志物和治疗靶点的潜力。
3. **"Recombinant FN14 extracellular domain attenuates liver fibrosis in mice"**
*Saitoh, T. et al. (2019), Biochemical Journal*
摘要：通过重组FN14胞外域蛋白阻断TWEAK-FN14相互作用，显著减轻小鼠肝纤维化模型中的胶原沉积，证实FN14重组蛋白在纤维化疾病中的治疗应用价值。
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如需具体文献链接或补充，可提供研究方向进一步筛选!
TNFRSF12A, also known as FN14 (Fibroblast growth factor-inducible 14) or TWEAKR (TNF-related weak inducer of apoptosis receptor), is a member of the tumor necrosis factor receptor superfamily (TNFRSF). This type I transmembrane protein consists of a small extracellular domain containing a cysteine-rich region (CRD) critical for ligand binding, a transmembrane helix, and a short intracellular domain. It was initially identified as a gene induced by fibroblast growth factors (FGFs) in endothelial cells, but later studies revealed its broader expression in tissues like the liver, kidney, and immune cells.
The primary ligand for TNFRSF12A is TWEAK (TNFSF12), and their interaction activates downstream signaling pathways, including NF-κB and MAPK, regulating cellular processes such as proliferation, migration, inflammation, and apoptosis. TNFRSF12A is involved in tissue remodeling, fibrosis, and pathological conditions like cancer, chronic inflammatory diseases, and neurodegenerative disorders. Its overexpression in solid tumors correlates with tumor progression, metastasis, and therapy resistance, making it a potential therapeutic target.
Recombinant TNFRSF12A protein is typically produced in mammalian or insect expression systems to preserve post-translational modifications and ligand-binding capacity. It serves as a critical tool for studying receptor-ligand interactions, screening inhibitors, and developing antibody-based therapies. In therapeutic research, targeting TNFRSF12A with monoclonal antibodies or fusion proteins aims to modulate aberrant signaling in diseases like fibrosis or cancer. However, its dual roles in tissue repair and pathological inflammation require precise targeting strategies to balance therapeutic efficacy and safety.
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