纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | TRAF2 |
Uniprot No | Q12933 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-501aa |
氨基酸序列 | MAAASVTPPGSLELLQPGFSKTLLGTKLEAKYLCSACRNVLRRPFQAQCG HRYCSFCLASILSSGPQNCAACVHEGIYEEGISILESSSAFPDNAARREV ESLPAVCPSDGCTWKGTLKEYESCHEGRCPLMLTECPACKGLVRLGEKER HLEHECPERSLSCRHCRAPCCGADVKAHHEVCPKFPLTCDGCGKKKIPRE KFQDHVKTCGKCRVPCRFHAIGCLETVEGEKQQEHEVQWLREHLAMLLSS VLEAKPLLGDQSHAGSELLQRCESLEKKTATFENIVCVLNREVERVAMTA EACSRQHRLDQDKIEALSSKVQQLERSIGLKDLAMADLEQKVLEMEASTY DGVFIWKISDFARKRQEAVAGRIPAIFSPAFYTSRYGYKMCLRIYLNGDG TGRGTHLSLFFVVMKGPNDALLRWPFNQKVTLMLLDQNNREHVIDAFRPD VTSSSFQRPVNDMNIASGCPLFCPVSKMEAKNSYVRDDAIFIKAIVDLTG L |
预测分子量 | 89 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TRAF2重组蛋白的3篇代表性文献:
1. **"TRAF2 Is Essential for JNK but Not NF-κB Activation and Regulates Lymphocyte Proliferation and Apoptosis"**
- **作者**: Yeh, W.C. et al. (1997)
- **摘要**: 本研究利用重组TRAF2蛋白及基因敲除模型,揭示TRAF2在JNK信号通路激活中的关键作用,但对NF-κB的激活并非必需,并发现其通过调控细胞凋亡影响淋巴细胞存活。
2. **"Structural Basis for the Interaction of TAK1 with TRAF2 in NF-κB Signaling"**
- **作者**: Yin, Q. et al. (2015)
- **摘要**: 通过重组TRAF2蛋白的体外结合实验和X射线晶体学分析,阐明了TRAF2与TAK1激酶的相互作用机制,揭示了其通过特定结构域介导下游NF-κB信号传导的结构基础。
3. **"TRAF2 Must Bind to Cellular Inhibitors of Apoptosis (cIAPs) for TNF-Mediated NF-κB Activation"**
- **作者**: Vince, J.E. et al. (2009)
- **摘要**: 利用重组TRAF2和cIAP1/2蛋白的共表达系统,证明TRAF2需与cIAPs形成复合物才能激活NF-κB,揭示了其在肿瘤坏死因子(TNF)信号中的依赖性调控机制。
4. **"Recombinant TRAF2 Protein Demonstrates E3 Ubiquitin Ligase Activity in vitro"**
- **作者**: Shi, J.H. et al. (2016)
- **摘要**: 通过体外泛素化实验,证实重组TRAF2蛋白具有E3泛素连接酶活性,并依赖其RING结构域促进底物泛素化,为研究TRAF2在炎症和癌症中的作用提供了生化证据。
(注:上述文献信息为示例,实际引用时请核对原文准确性。)
**Background of TRAF2 Recombinant Protein**
TRAF2 (TNF receptor-associated factor 2) is a critical adaptor protein involved in intracellular signaling pathways, primarily mediating signals from the tumor necrosis factor receptor (TNFR) superfamily and Toll-like receptors (TLRs). It plays a central role in regulating immune responses, cell survival, apoptosis, and inflammation by activating downstream effectors such as NF-κB and MAPK pathways. Structurally, TRAF2 contains an N-terminal RING domain, which confers E3 ubiquitin ligase activity, followed by zinc finger motifs and a C-terminal TRAF domain responsible for protein-protein interactions.
Recombinant TRAF2 protein is engineered using expression systems (e.g., *E. coli* or mammalian cells) to produce purified, functional TRAF2 for research applications. This engineered protein retains key domains necessary for binding upstream receptors (e.g., TNFR1/2) and downstream signaling components (e.g., cIAPs, RIP1). Researchers utilize recombinant TRAF2 to study its role in signal transduction mechanisms, particularly in contexts like inflammation, cancer, and autoimmune diseases. For example, TRAF2 is implicated in resisting apoptosis in certain cancers by promoting NF-κB-driven survival signals, making it a potential therapeutic target.
Additionally, recombinant TRAF2 is employed in *in vitro* assays to map interaction networks, assess ubiquitination dynamics, and screen inhibitors aiming to modulate TRAF2-dependent pathways. Its study has also revealed dual roles in cell death regulation, as TRAF2 can either inhibit apoptosis via NF-κB activation or facilitate necroptosis under specific conditions. Overall, TRAF2 recombinant protein serves as a vital tool for dissecting complex signaling cascades and developing targeted therapies for diseases linked to dysregulated immune or apoptotic signaling.
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