| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NRAS |
| Uniprot No | P01111 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-186aa |
| 氨基酸序列 | MTEYKLVVVGAGGVGKSALTIQLIQNHFVDEYDPTIEDSYRKQVVIDGETCLLDILDTAGQEEYSAMRDQYMRTGEGFLCVFAINNSKSFADINLYREQIKRVKDSDDVPMVLVGNKCDLPTRTVDTKQAHELAKSYGIPFIETSAKTRQGVEDAFYTLVREIRQYRMKKLNSSDDGTQGCMGLPC |
| 预测分子量 | 56.1 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NRAS重组蛋白的3篇参考文献：
1. **《Mutant NRAS has oncogenic properties equivalent to activated KRAS》** - Smith, M.J., et al.
摘要：该研究通过重组NRAS蛋白实验，证明NRAS突变体在体外和细胞模型中与KRAS类似，能够激活MAPK信号通路并促进细胞转化，揭示了NRAS在癌症中的直接致癌机制。
2. **《Structural and biochemical characterization of the recombinant NRAS protein》** - Johnson, L., et al.
摘要：作者利用大肠杆菌表达系统纯化重组NRAS蛋白，并通过X射线晶体学解析其结构，揭示了其GTP结合区域的构象变化，为靶向NRAS的药物设计提供了结构基础。
3. **《Targeting NRAS mutations in melanoma through recombinant protein-based drug screening》** - Chen, Z., et al.
摘要：研究构建了重组NRAS突变蛋白(如Q61K)，并基于此开发高通量药物筛选平台，鉴定出多个小分子化合物可抑制NRAS-RAF相互作用，为黑色素瘤治疗提供潜在策略。
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注：以上文献信息为示例性质，具体文献需通过学术数据库检索确认。
**Background of NRAS Recombinant Protein**
The NRAS (Neuroblastoma RAS viral oncogene homolog) gene encodes a member of the RAS GTPase family, pivotal in regulating cell signaling pathways that control proliferation, differentiation, and survival. NRAS functions as a molecular switch, cycling between active GTP-bound and inactive GDP-bound states. It transmits signals from cell surface receptors (e.g., growth factor receptors) to intracellular effectors, primarily through the RAS-MAPK pathway. Mutations in NRAS, commonly at codons 12. 13. or 61. impair GTP hydrolysis, leading to constitutive activation. Such mutations are oncogenic drivers in cancers like melanoma, leukemia, and colorectal carcinoma.
Recombinant NRAS proteins are engineered in vitro using expression systems (e.g., *E. coli* or mammalian cells) to produce purified, functional proteins for research. These proteins retain critical domains, including the GTP-binding region and effector interaction sites, enabling studies on NRAS biochemistry and mutation-driven dysregulation. Researchers utilize recombinant NRAS to investigate its role in oncogenesis, screen for inhibitors, and validate therapeutic targets.
The development of recombinant NRAS has advanced understanding of RAS-driven cancers and facilitated drug discovery, particularly for therapies targeting hyperactive NRAS mutants. Despite challenges in directly inhibiting RAS proteins, recombinant forms aid in exploring alternative strategies, such as disrupting RAS-membrane interactions or targeting downstream effectors. This tool remains essential for unraveling NRAS biology and developing precision oncology approaches.
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