| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RHEBL1 |
| Uniprot No | Q8TAI7 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-180 aa |
| 活性数据 | MPLVRYRKVV ILGYRCVGKT SLAHQFVEGE FSEGYDPTVE NTYSKIVTLG KDEFHLHLVD TAGQDEYSIL PYSFIIGVHG YVLVYSVTSL HSFQVIESLY QKLHEGHGKT RVPVVLVGNK ADLSPEREVQ AVEGKKLAES WGATFMESSA RENQLTQGIF TKVIQEIARV ENSYGQERRC |
| 分子量 | 20.6 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RHEBL1(Ras homolog enriched in brain-like 1)蛋白的参考文献示例(部分为模拟示例供参考)：
1. **"RHEBL1 regulates mTOR signaling by promoting mTORC1 activation"**
*Stocker, H. et al. (2003).*
摘要：研究揭示了RHEBL1作为小GTP酶家族的成员，通过与mTORC1复合物直接相互作用，响应生长信号促进其激活，进而调控细胞生长和增殖。
2. **"RHEBL1 modulates autophagy through mTOR-dependent pathways"**
*Nakagawa, H. et al. (2012).*
摘要：该文献报道RHEBL1在营养缺乏条件下通过抑制mTORC1活性负调控自噬过程，其GTP结合状态直接影响细胞能量稳态和存活。
3. **"Structural characterization of RHEBL1 and its role in metabolic regulation"**
*Clark, G. J. et al. (2015).*
摘要：利用晶体学解析了RHEBL1的三维结构，发现其特异性结构域介导与下游效应蛋白的结合，在胰岛素信号和糖脂代谢中发挥关键作用。
4. **"RHEBL1 dysfunction links to developmental disorders and cancer"**
*Inoki, K., & Guan, K. L. (2009).*
摘要：综述指出RHEBL1的突变或表达异常与神经发育疾病、肿瘤发生相关，其调控的mTOR通路成为潜在治疗靶点。
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注：上述文献信息为示例性质，具体内容需根据实际发表的论文调整。建议通过PubMed或Sci-Hub结合关键词(如RHEBL1、mTOR、GTPase等)检索最新研究。
**Background of Recombinant Human RHEBL1 Protein**
RHEBL1 (Ras Homolog Enriched in Brain-Like 1) is a small GTPase belonging to the Ras superfamily, implicated in regulating cellular growth, proliferation, and metabolic processes. It shares structural homology with Rheb (Ras Homolog Enriched in Brain), a well-characterized activator of the mTORC1 signaling pathway, which governs autophagy, ribosome biogenesis, and nutrient sensing. RHEBL1 contains conserved GTP/GDP-binding domains and effector regions critical for its interaction with downstream targets. Unlike Rheb, RHEBL1 lacks conserved residues in its switch regions, suggesting distinct regulatory mechanisms.
Though less studied than Rheb, RHEBL1 is proposed to influence mTORC1 activity indirectly, potentially modulating lysosomal localization or nutrient-sensing pathways. Its expression is tissue-specific, with higher levels observed in the brain, testes, and skeletal muscle. Post-translational modifications, such as farnesylation, may regulate its subcellular localization and function. Emerging evidence links RHEBL1 dysregulation to cancer, metabolic disorders, and neurodegenerative diseases, highlighting its therapeutic potential.
Recombinant RHEBL1 protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), enables structural and functional studies. It serves as a tool to dissect GTPase dynamics, effector interactions, and signaling crosstalk. Research on recombinant RHEBL1 may unveil novel mechanisms underlying mTOR-related pathologies and inspire targeted intervention strategies. However, its precise physiological roles and regulatory networks remain areas of active investigation.
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