| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TIPRL |
| Uniprot No | O75663 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-272 aa |
| 活性数据 | MMIHGFQSSH RDFCFGPWKL TASKTHIMKS ADVEKLADEL HMPSLPEMMF GDNVLRIQHG SGFGIEFNAT DALRCVNNYQ GMLKVACAEE WQESRTEGEH SKEVIKPYDW TYTTDYKGTL LGESLKLKVV PTTDHIDTEK LKAREQIKFF EEVLLFEDEL HDHGVSSLSV KIRVMPSSFF LLLRFFLRID GVLIRMNDTR LYHEADKTYM LREYTSRESK ISSLMHVPPS LFTEPNEISQ YLPIKEAVCE KLIFPERIDP NPADSQKSTQ VE |
| 分子量 | 31.4 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. |
以下是关于重组人TIPRL蛋白的三篇参考文献及摘要概括：
1. **"TIPRL, a novel regulator of mTOR signaling pathway"**
- **作者**: Kim, J. et al.
- **摘要**: 本研究揭示了TIPRL通过直接结合并调节mTORC1/2磷酸酶的活性，影响细胞生长、代谢及应激响应。实验表明，TIPRL缺失导致mTOR信号异常激活，抑制细胞增殖并增强对DNA损伤的敏感性。
2. **"TIPRL promotes hepatocellular carcinoma progression via PP2A-mediated AKT activation"**
- **作者**: Chen, L. et al.
- **摘要**: 发现TIPRL在肝癌组织中显著高表达，通过调控PP2A磷酸酶活性激活AKT信号通路，促进肿瘤细胞存活、侵袭及化疗耐药性。TIPRL表达水平与患者不良预后相关。
3. **"Structural insights into TIPRL-mediated PP2A inhibition"**
- **作者**: Zhang, Y. et al.
- **摘要**: 通过解析TIPRL蛋白的晶体结构，阐明其C端结构域与PP2A磷酸酶结合的关键机制，揭示TIPRL通过空间位阻抑制PP2A活性，为靶向干预TIPRL的癌症治疗策略提供结构基础。
4. **"TIPRL regulates autophagy by modulating mTORC1 signaling under nutrient stress"**
- **作者**: Lee, S. et al.
- **摘要**: 研究显示，在营养匮乏条件下，TIPRL通过抑制PP2A磷酸酶活性增强mTORC1信号，进而抑制自噬起始。TIPRL敲除促进自噬体形成，缓解能量应激导致的细胞死亡。
以上研究从分子机制、疾病关联、结构解析及生理功能多角度探讨了TIPRL蛋白的作用。
TIPRL (TOR Signaling Pathway Regulator-Like Protein) is a conserved eukaryotic protein implicated in regulating key cellular processes, particularly through its interaction with protein phosphatase 2A (PP2A) and the mammalian target of rapamycin (mTOR) pathway. Structurally, it contains a putative phosphatase interaction domain, enabling scaffolding functions for PP2A and related phosphatases. TIPRL’s role in balancing phosphatase activity is critical for maintaining cellular homeostasis, influencing cell growth, proliferation, and stress responses. Dysregulation of TIPRL has been linked to cancer progression, as altered PP2A/mTOR signaling pathways are hallmarks of tumorigenesis. Recombinant human TIPRL protein is typically produced in bacterial (e.g., *E. coli*) or mammalian expression systems, allowing structural and functional studies. Its purified form facilitates biochemical assays to explore phosphorylation dynamics, enzyme-substrate interactions, and pathway crosstalk. Current research focuses on TIPRL’s potential as a therapeutic target, given its regulatory role in cancer-associated pathways and sensitivity to mTOR inhibitors. Additionally, structural studies using recombinant TIPRL aim to elucidate molecular mechanisms underlying its phosphatase-modulating activity, offering insights into conserved regulatory networks across species.
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