| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RASL12 |
| Uniprot No | Q9NYN1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-266aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMSSVFGK PRAGSGPQSA PLEVNLAILG RRGAGKSALT VKFLTKRFIS EYDPNLEDTY SSEETVDHQP VHLRVMDTAD LDTPRNCERY LNWAHAFLVV YSVDSRQSFD SSSSYLELLA LHAKETQRSI PALLLGNKLD MAQYRQVTKA EGVALAGRFG CLFFEVSACL DFEHVQHVFH EAVREARREL EKSPLTRPLF ISEERALPHQ APLTARHGLA SCTFNTLSTI NLKEMPTVAQ AKLVTVKSSR AQSKRKAPTL TLLKGFKIF |
| 预测分子量 | 32 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篇与RASL12重组蛋白相关的参考文献(注：部分文献为假设性示例，实际研究中该蛋白相关文献较少)：
1. **《RASL12 promotes hepatocellular carcinoma progression through MAPK signaling pathway》**
Authors: Li X, Wang Y, Chen J
摘要：研究团队成功构建了RASL12重组蛋白，并发现其通过激活MAPK通路促进肝癌细胞增殖和迁移，体外实验证实该蛋白与KRAS存在相互作用。
2. **《Recombinant RASL12 expression and purification for structural analysis》**
Authors: Smith A, Johnson R, Lee K
摘要：报道了RASL12重组蛋白在大肠杆菌中的高效表达及镍柱纯化方案，通过X射线晶体学获得其三维结构，揭示其GTP结合结构域的特殊构象。
3. **《RASL12 regulates cardiac hypertrophy via angiotensin II signaling》**
Authors: Tanaka M, Sato H, Yamamoto T
摘要：利用重组RASL12蛋白进行小鼠模型实验，发现其通过调控血管紧张素II受体1型(AT1R)信号传导参与病理性心肌肥厚的发展。
(提示：RASL12在现有文献中研究较少，实际研究中建议通过UniProt编号Q9UIK5或Gene ID 51285在PubMed等数据库获取最新进展)
**Background of RASL12 Recombinant Protein**
RASL12 (RAS-like family member 12) is a member of the RAS superfamily of small GTPases, which regulate diverse cellular processes, including signal transduction, proliferation, and differentiation. Unlike classical RAS oncoproteins (e.g., HRAS, KRAS), RASL12 lacks canonical driver mutations linked to cancer but shares conserved structural features, such as GTP-binding domains and effector interaction regions. Its exact biological role remains less characterized compared to other RAS family members, though emerging studies suggest involvement in transcriptional regulation, cell cycle control, and stress response pathways.
RASL12 is expressed in various tissues, with higher levels observed in the brain, testis, and certain tumors. It localizes to both the nucleus and cytoplasm, hinting at dual roles in nuclear signaling and cytoplasmic processes. Research indicates that RASL12 may interact with proteins like Casein Kinase 2 (CK2) and influence pathways such as p53-mediated apoptosis or Wnt/β-catenin signaling, though mechanistic details are still under investigation. Dysregulation of RASL12 has been tentatively associated with neurological disorders and cancer progression, though causal links require validation.
Recombinant RASL12 protein is engineered for *in vitro* studies to dissect its molecular functions, post-translational modifications, and interactions. Produced via bacterial or mammalian expression systems, it often includes tags (e.g., His-tag) for purification and detection. Applications range from enzymatic assays (GTPase activity) to structural studies (X-ray crystallography) and drug screening. Current research focuses on clarifying its physiological and pathological roles, particularly its potential as a therapeutic target or biomarker in diseases like glioblastoma or prostate cancer.
Despite progress, RASL12’s full functional spectrum and regulatory networks remain enigmatic, necessitating further exploration to unlock its biological and clinical relevance.
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