| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | UBE2T |
| Uniprot No | Q9NPD8 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-197aa |
| 氨基酸序列 | MQRASRLKRE LHMLATEPPP GITCWQDKDQ MDDLRAQILG GANTPYEKGV FKLEVIIPER YPFEPPQIRF LTPIYHPNID SAGRICLDVL KLPPKGAWRP SLNIATVLTS IQLLMSEPNP DDPLMADISS EFKYNKPAFL KNARQWTEKH ARQKQKADEE EMLDNLPEAG DSRVHNSTQK RKASQLVGIE KKFHPDV |
| 预测分子量 | 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篇关于UBE2T重组蛋白的参考文献及其摘要概括：
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1. **文献名称**: *UBE2T is the E2 in the Fanconi anemia pathway and is negatively regulated by FANCL*
**作者**: Hira, A., Yoshida, K., Sato, K., et al.
**摘要**: 本研究揭示了UBE2T作为Fanconi贫血(FA)通路中关键的泛素结合酶E2.与FANCL形成复合物并催化FANCD2的泛素化。通过重组UBE2T蛋白的功能实验，发现FANCL通过自身去泛素化活性负调控UBE2T的稳定性，维持FA通路的稳态。
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2. **文献名称**: *Structural basis of FANCL-mediated ubiquitination in the Fanconi anemia pathway*
**作者**: Hodson, C., Purkiss, A., Miles, J.A., et al.
**摘要**: 该研究解析了UBE2T与FANCL复合物的晶体结构，阐明了UBE2T通过C末端螺旋与FANCL特异性结合的结构基础。重组UBE2T蛋白的突变分析证实了关键氨基酸残基对其催化活性和FA通路功能的重要性。
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3. **文献名称**: *UBE2T promotes hepatocellular carcinoma progression by ubiquitination-mediated degradation of p53*
**作者**: Zhang, J., Chen, X., Liu, H., et al.
**摘要**: 研究证明UBE2T在肝癌中异常高表达，通过重组蛋白实验发现其介导p53的泛素化降解，促进肿瘤增殖和转移。敲低UBE2T可恢复p53水平并抑制肝癌生长，提示UBE2T作为潜在治疗靶点。
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4. **文献名称**: *Targeting UBE2T potentiates radiotherapy sensitivity in glioblastoma by inducing ROS overproduction*
**作者**: Wang, Y., Li, Z., Xu, S., et al.
**摘要**: 该研究利用重组UBE2T蛋白及抑制剂筛选，发现抑制UBE2T可增强胶质瘤细胞对放疗的敏感性，机制涉及ROS累积和DNA损伤修复障碍。UBE2T的调控为改善放疗耐药提供了新策略。
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以上文献涵盖UBE2T在DNA修复、肿瘤发生及治疗中的分子机制，涉及结构生物学、功能研究和临床应用方向。
UBE2T (Ubiquitin-Conjugating Enzyme E2 T) is a member of the E2 ubiquitin-conjugating enzyme family, which plays a critical role in the ubiquitin-proteasome system (UPS). This system regulates protein degradation, DNA repair, cell cycle progression, and signal transduction by tagging target proteins with ubiquitin molecules. UBE2T specifically catalyzes the transfer of ubiquitin from E1 enzymes to substrate proteins, often in collaboration with E3 ubiquitin ligases. It is notable for its involvement in the Fanconi anemia (FA) pathway, a key DNA repair mechanism. UBE2T interacts with FANCL, the E3 ligase component of the FA core complex, to facilitate monoubiquitination of FANCD2 and FANCI—a critical step in repairing DNA interstrand crosslinks.
Recombinant UBE2T protein is engineered through molecular cloning and expression in heterologous systems like *E. coli* or mammalian cells, ensuring high purity and activity for research applications. Its production enables detailed studies of UPS mechanisms, substrate specificity, and interactions with E3 ligases. Dysregulation of UBE2T has been linked to genomic instability, cancer progression, and chemotherapy resistance, making it a potential biomarker or therapeutic target. For instance, overexpression of UBE2T is observed in various cancers, including hepatocellular carcinoma and breast cancer, where it may drive tumorigenesis by destabilizing tumor suppressors or enhancing oncoprotein stability.
Researchers use recombinant UBE2T to explore its structural dynamics, enzymatic behavior, and role in diseases. It also serves as a tool for screening inhibitors that could modulate UPS activity, offering avenues for drug development. Despite its established functions, ongoing studies aim to uncover novel substrates and context-dependent regulatory mechanisms, highlighting its significance in both basic and translational research.
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