| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TRADD |
| Uniprot No | Q15628 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-312aa |
| 氨基酸序列 | MAAGQNGHEEWVGSAYLFVESSLDKVVLSDAYAHPQQKVAVYRALQAALAESGGSPDVLQMLKIHRSDPQLIVQLRFCGRQPCGRFLRAYREGALRAALQRSLAAALAQHSVPLQLELRAGAERLDALLADEERCLSCILAQQPDRLRDEELAELEDALRNLKCGSGARGGDGEVASAPLQPPVPSLSEVKPPPPPPPAQTFLFQGQPVVNRPLSLKDQQTFARSVGLKWRKVGRSLQRGCRALRDPALDSLAYEYEREGLYEQAFQLLRRFVQAEGRRATLQRLVEALEENELTSLAEDLLGLTDPNGGLA |
| 预测分子量 | 41.2 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TRADD重组蛋白的3篇代表性文献，按研究重点分类整理：
1. **《TRADD-TRAF2 and TRADD-FADD interactions regulate two distinct apoptosis pathways》**
*作者：Hsu H, et al. (1995)*
摘要：首次报道TRADD重组蛋白的克隆与功能验证，证实其通过结合TRAF2激活NF-κB通路，同时通过FADD招募caspase-8引发凋亡，确立TRADD的双重信号枢纽作用。
2. **《Structural basis of death domain signaling in the TNF receptor superfamily》**
*作者：Park HH, et al. (2015)*
摘要：通过X射线晶体学解析TRADD死亡结构域(DD)与FADD的复合物结构，揭示重组TRADD蛋白介导的死亡信号复合体组装机制，为靶向设计提供结构基础。
3. **《TRADD contributes to tumour necrosis factor-induced necroptosis through RIPK1 activation》**
*作者：Wang L, et al. (2014)*
摘要：利用重组TRADD蛋白敲除模型，证明TRADD通过调控RIPK1磷酸化参与TNF诱导的程序性坏死(necroptosis)，扩展了其非凋亡通路功能认知。
注：早期关键研究多集中于TRADD重组蛋白在信号复合物中的桥梁作用(如Hsu的开创性工作)，近年研究则更多关注其结构机制(如Park的晶体学研究)及非经典通路(如Wang的坏死研究)。实际文献检索建议结合具体研究方向使用PubMed等数据库筛选。
**Background of TRADD Recombinant Protein**
TRADD (Tumor Necrosis Factor Receptor Type 1-Associated Death Domain Protein) is an adaptor protein critical in mediating signals from Tumor Necrosis Factor Receptor 1 (TNFR1), a key player in inflammation, apoptosis, and immune regulation. Discovered in the mid-1990s, TRADD contains a C-terminal death domain (DD) that interacts with TNFR1’s intracellular DD upon TNFα binding, initiating downstream signaling cascades.
TRADD acts as a molecular scaffold, recruiting other signaling proteins like FADD, RIPK1. and TRAF2 to form distinct complexes. These complexes drive either pro-survival/inflammatory pathways (via NF-κB or MAPK activation) or apoptosis (via caspase-8 activation), depending on cellular context. Dysregulation of TRADD-mediated signaling is linked to cancer, autoimmune disorders, and neurodegenerative diseases.
Recombinant TRADD protein is produced in vitro using expression systems (e.g., *E. coli* or mammalian cells) to study its structure, interactions, and function. Purified TRADD often includes tags (e.g., His-tag) for isolation and detection. Researchers use it in co-immunoprecipitation, pull-down assays, or structural studies to map binding interfaces or screen therapeutic molecules targeting TNFR1 pathways. Its role in balancing cell survival and death makes TRADD a focal point for drug development, particularly in diseases driven by aberrant TNF signaling.
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