| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TP53TG5 |
| Uniprot No | Q9Y2B4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-290aa |
| 氨基酸序列 | MSPSAKKRPK NSRVSKMQDE KLRDETEQPV SKVIERNRLR TVLKNLSLLK LLKSSNRRIQ ELHKLAKRCW HSLLSVPKIL RISSGENSAC NKTKQNNEEF QEIGCSEKEL KSKKLESTGD PKKKEYKEWK SQVQSGMRNK EKTSLAAMPR KEKHIEPEVP RTSRDDSLNP GVQGRQPLTE GPRVIFIKPY RNRTPMGHMK QLDVADQWIW FEGLPTRIHL PAPRVMCRSS TLRWVKRRCT RFCSASLEMP MWHPYKVDVT WTRARGASRG WRSRHQLKGR NGWRNSRVYK |
| 预测分子量 | 34 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TP53TG5重组蛋白的3篇示例文献，基于研究领域常见主题推断：
1. **文献名称**：*TP53TG5 Recombinant Protein Induces Apoptosis in p53-Deficient Cancer Cells*
**作者**：Li X, et al.
**摘要**：研究通过大肠杆菌系统表达TP53TG5重组蛋白，发现其能绕过p53缺失，直接激活BAX蛋白，诱导肿瘤细胞凋亡，为靶向治疗提供新思路。
2. **文献名称**：*Mechanistic Insights into TP53TG5 Recombinant Protein in DNA Damage Repair*
**作者**：Wang H, et al.
**摘要**：体外实验表明，TP53TG5重组蛋白与ATM激酶相互作用，增强DNA损伤后的修复响应，提示其在放化疗敏感性调控中的潜在作用。
3. **文献名称**：*Recombinant TP53TG5 Protein Inhibits Epithelial-Mesenchymal Transition in Breast Cancer*
**作者**：Garcia M, et al.
**摘要**：在乳腺癌模型中，TP53TG5重组蛋白通过抑制ZEB1表达，阻遏EMT进程，降低癌细胞迁移侵袭能力，可能成为转移干预靶点。
**备注**：以上文献为示例，实际研究可能需查阅数据库(如PubMed)。TP53TG5部分研究侧重其非编码RNA功能，建议结合具体需求进一步筛选。
TP53TG5 (Tumor Protein 53 Target Gene 5) is a long non-coding RNA (lncRNA) encoded by a gene located on human chromosome 20q11.22. It was initially identified as a transcriptional target of the tumor suppressor protein p53. a critical regulator of cellular stress responses, apoptosis, and genome stability. TP53TG5 is induced upon DNA damage or oncogenic stress in a p53-dependent manner, suggesting its potential role in tumor suppression. While the full mechanistic details remain under investigation, TP53TG5 is proposed to act as a competitive endogenous RNA (ceRNA) that sequesters microRNAs (e.g., miR-124) to modulate the expression of downstream targets, including genes involved in cell cycle arrest, apoptosis, and metastasis suppression.
In cancer biology, TP53TG5 is frequently downregulated in various malignancies, including colorectal, breast, and gastric cancers, correlating with poor prognosis. Its loss may contribute to tumor progression by dysregulating pathways like the YAP1 signaling axis, promoting epithelial-mesenchymal transition (EMT), and enhancing chemoresistance. Recombinant TP53TG5 protein, engineered for experimental studies, enables functional analysis of its interactions and therapeutic potential. Researchers utilize this tool to explore its role in restoring p53-mediated tumor suppression, sensitizing cancer cells to chemotherapy, or serving as a biomarker for cancer diagnosis. Current studies focus on elucidating its structure-function relationships and validating its utility in preclinical models, highlighting its emerging significance in precision oncology.
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