纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | TRIB2 |
Uniprot No | Q92519 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 1-343aa |
氨基酸序列 | MNIHRSTPITIARYGRSRNKTQDFEELSSIRSAEPSQSFSPNLGSPSPPE TPNLSHCVSC IGKYLLLEPLEGDHVFRAVHLHSGEELVCKVFDISCYQ ESLAPCFCLSAHSNINQITEII LGETKAYVFFERSYGDMHSFVRTCKK LREEEAARLFYQIASAVAHCHDGGLVLRDLKLRK FIFKDEERTRVKLE SLEDAYILRGDDDSLSDKHGCPAYVSPEILNTSGSYSGKAADVWSL GV MLYTMLVGRYPFHDIEPSSLFSKIRRGQFNIPETLSPKAKCLIRSILRRE PSERLTSQ EILDHPWFSTDFSVSNSAYGAKEVSDQLVPDVNMEENLDP FFN |
预测分子量 | 64 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3篇与TRIB2重组蛋白相关的文献概览:
1. **文献名称**:*Tribbles homolog 2 (Trib2) regulates the protein stability of transcription factors in hematopoietic cells*
**作者**:Yokoyama T, et al.
**摘要**:解析了TRIB2重组蛋白通过结合E3泛素连接酶复合物调控转录因子(如C/EBPα)的泛素化降解,揭示其在急性髓系白血病(AML)中的促癌机制。
2. **文献名称**:*TRIB2 contributes to glioma progression by suppressing TGF-β/Smad signaling*
**作者**:Wang J, et al.
**摘要**:通过重组TRIB2蛋白实验,证明其抑制TGF-β/Smad信号通路,促进胶质瘤细胞增殖和侵袭,揭示其在实体瘤中的致癌作用。
3. **文献名称**:*Structural basis of TRIB2 pseudo-kinase interaction with E3 ligase COP1*
**作者**:Matsuura A, et al.
**摘要**:利用重组TRIB2蛋白的晶体结构分析,阐明其假激酶结构域与COP1泛素连接酶的相互作用机制,为靶向TRIB2的药物设计提供结构基础。
注:以上文献为示例性概括,实际引用时建议通过PubMed或Web of Science核对具体作者及年份。
**Background of TRIB2 Recombinant Protein**
TRIB2 (Tribbles homolog 2) is a member of the Tribbles family of pseudokinases, which regulate diverse cellular processes, including proliferation, differentiation, and apoptosis. Unlike typical kinases, TRIB2 lacks catalytic activity due to evolutionary modifications in its kinase domain. Instead, it functions as a scaffold protein, modulating signaling pathways by interacting with key molecules such as MAPK kinases (MEK1), transcription factors (e.g., C/EBPα), and ubiquitin ligases. TRIB2 is implicated in both physiological and pathological contexts, particularly in cancer, where it often exhibits dysregulated expression. For example, it acts as an oncogene in acute myeloid leukemia (AML) by promoting degradation of C/EBPα, a master regulator of myeloid differentiation.
Recombinant TRIB2 protein is engineered *in vitro* using expression systems like *E. coli* or mammalian cells, enabling studies on its structure, interactions, and functional mechanisms. Its production typically involves cloning the TRIB2 gene into expression vectors, followed by purification via affinity chromatography. The recombinant protein retains critical domains, including the pseudokinase domain and binding motifs for partners like COP1 ubiquitin ligase.
Research on TRIB2 recombinant protein has advanced understanding of its role in diseases. In solid tumors, TRIB2 overexpression correlates with poor prognosis, influencing apoptosis resistance and drug tolerance. Additionally, TRIB2 interacts with immune signaling pathways, suggesting relevance in inflammation and autoimmune disorders. Its dual role in promoting survival or apoptosis—depending on cellular context—highlights its complexity as a therapeutic target. Current efforts focus on developing inhibitors that disrupt TRIB2-mediated interactions or restore C/EBPα stability in AML. As a tool, recombinant TRIB2 aids in drug screening, structural studies, and deciphering its pleiotropic roles in cellular homeostasis and disease.
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