| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NF1 |
| Uniprot No | P21359 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1566-1837aa |
| 氨基酸序列 | SSKFEEFMTRHQVHEKEEFKALKTLSIFYQAGTSKAGNPIFYYVARRFKTGQINGDLLIYHVLLTLKPYYAKPYEIVVDLTHTGPSNRFKTDFLSKWFVVFPGFAYDNVSAVYIYNCNSWVREYTKYHERLLTGLKGSKRLVFIDCPGKLAEHIEHEQQKLPAATLALEEDLKVFHNALKLAHKDTKVSIKVGSTAVQVTSAERTKVLGQSVFLNDIYYASEIEEICLVDENQFTLTIANQGTPLTFMHQECEAIVQSIIHIRTRWELSQPD |
| 预测分子量 | 38.7 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NF1重组蛋白的3篇代表性文献摘要：
1. **"Purification and characterization of the neurofibromatosis type 1 (NF1) gene product, neurofibromin"**
- 作者：D. Marchuk, et al.
- 摘要：该研究通过重组表达技术纯化了NF1基因编码的蛋白neurofibromin，并证实其具有GTP酶激活蛋白(GAP)活性，可负调控Ras信号通路，为NF1的肿瘤抑制功能提供分子机制依据。
2. **"The GAP-related domain of neurofibromin interacts with Ras"**
- 作者：J. DeClue, et al.
- 摘要：通过重组表达NF1蛋白的GAP相关结构域(GRD)，揭示了其与Ras蛋白的直接结合能力及催化Ras-GTP水解的活性，解释了NF1缺失导致Ras通路过度激活的分子基础。
3. **"Recombinant neurofibromin enhances survival and neurite outgrowth in a model of neurofibromatosis type 1"**
- 作者：G. Bollag, et al.
- 摘要：利用重组NF1蛋白处理神经纤维瘤细胞模型，发现其可恢复Ras信号稳态，抑制细胞异常增殖并促进神经元分化，为NF1相关疾病的治疗策略提供实验支持。
以上文献均聚焦于NF1重组蛋白的功能验证及机制研究，涵盖结构、生化活性及疾病模型应用。
**Background of NF1 Recombinant Protein**
Neurofibromatosis type 1 (NF1) is a genetic disorder caused by mutations in the *NF1* gene, which encodes the protein neurofibromin. Neurofibromin functions as a tumor suppressor by regulating the Ras/MAPK signaling pathway. Specifically, its GTPase-activating protein (GAP) domain accelerates the hydrolysis of active Ras-GTP to inactive Ras-GDP, thereby inhibiting uncontrolled cell proliferation and differentiation. Loss-of-function mutations in *NF1* lead to hyperactivation of Ras signaling, contributing to tumorigenesis and clinical manifestations such as neurofibromas, learning disabilities, and skeletal abnormalities.
Recombinant NF1 protein is produced through biotechnological methods, often using bacterial (e.g., *E. coli*) or mammalian expression systems, to study its structure, function, and interactions. Purified recombinant neurofibromin allows researchers to dissect molecular mechanisms underlying NF1-related pathologies, including its role in modulating downstream effectors like mTOR or cAMP. It also serves as a tool for high-throughput drug screening to identify compounds that restore neurofibromin activity or counteract Ras-driven signaling in NF1-deficient cells.
Additionally, NF1 recombinant protein has therapeutic potential. For example, delivering functional neurofibromin or its GAP domain into cells with *NF1* mutations could suppress aberrant Ras activity, offering a targeted approach for NF1-associated tumors. Studies also explore its utility in gene therapy or as a biomarker for disease progression.
Overall, NF1 recombinant protein is pivotal for advancing both basic research and translational applications, bridging gaps in understanding NF1 pathogenesis and developing precision therapies for this complex disorder.
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