| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RGS5 |
| Uniprot No | O15539 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-181aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSHMCKGLAALPHSCLERAKEIKIKLGIL LQKPDSVGDLVIPYNEKPEKPAKTQKTSLDEALQWRDSLDKLLQNNYGLA SFKSFLKSEFSEENLEFWIACEDYKKIKSPAKMAEKAKQIYEEFIQTEAP KEVNIDHFTKDITMKNLVEPSLSSFDMAQKRIHALMEKDSLPRFVRSEFY QELIK |
| 预测分子量 | 24 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RGS5重组蛋白的3-4篇参考文献及其摘要概括：
1. **"RGS5 as a Biomarker of Pericytes in Tumor Vasculature"**
- **作者**: Hamzah, J. et al.
- **摘要**: 该研究探讨RGS5在肿瘤相关周细胞中的高表达及其对血管成熟的影响。通过重组RGS5蛋白实验发现，RGS5缺失导致血管结构不稳定，促进肿瘤生长和转移，提示其作为抗血管生成治疗靶点的潜力。
2. **"RGS5 Deficiency Attenuates Hypoxia-induced Pulmonary Hypertension in Mice"**
- **作者**: Hao, X. et al.
- **摘要**: 研究利用RGS5敲除小鼠模型，发现RGS5通过调控G蛋白信号通路参与肺动脉高压的病理过程。重组RGS5蛋白实验表明，其表达减少可缓解血管重塑和血压升高，提示其在心血管疾病中的调控作用。
3. **"Structural Basis of RGS5-Mediated G Protein Inhibition"**
- **作者**: Chen, Z. et al.
- **摘要**: 通过X射线晶体学解析RGS5重组蛋白与Gα亚基的复合物结构，揭示其通过保守的RGS结构域加速Gα的GTP酶活性，阐明其在G蛋白信号通路中的分子机制，为靶向药物设计提供结构基础。
4. **"RGS5 Regulates Apoptosis in Vascular Smooth Muscle Cells"**
- **作者**: Wang, Y. et al.
- **摘要**: 研究显示RGS5重组蛋白通过抑制MAPK和AKT信号通路，调控血管平滑肌细胞凋亡，影响动脉粥样硬化进程。实验表明，RGS5过表达可促进细胞凋亡，为治疗血管增生性疾病提供新思路。
这些研究分别从肿瘤生物学、心血管病理、结构生物学及细胞凋亡机制角度，揭示了RGS5重组蛋白的功能多样性。
Regulator of G-protein Signaling 5 (RGS5) is a member of the RGS protein family, which plays a critical role in modulating G-protein-coupled receptor (GPCR) signaling pathways. As a GTPase-activating protein (GAP), RGS5 accelerates the hydrolysis of GTP bound to Gα subunits of heterotrimeric G-proteins, thereby terminating GPCR-mediated intracellular signaling. This regulatory function allows RGS5 to fine-tune cellular responses to extracellular stimuli, including hormones, neurotransmitters, and environmental signals. RGS5 is particularly noted for its involvement in vascular development, smooth muscle function, and tumor microenvironment regulation. Its expression is prominent in pericytes and vascular smooth muscle cells, where it influences blood vessel maturation and stability.
Recombinant RGS5 protein refers to the engineered version of this regulatory protein, typically produced in heterologous expression systems such as *E. coli* or mammalian cell cultures. The recombinant form retains the functional RGS domain responsible for GAP activity and may include affinity tags (e.g., His-tag) for purification and detection. Structural studies of recombinant RGS5 have revealed its conserved "RGS box" domain, which mediates interactions with activated Gα subunits, while its N- and C-terminal regions may contribute to subcellular localization or protein-protein interactions.
Research on recombinant RGS5 has advanced our understanding of its pathophysiological roles. Dysregulation of RGS5 has been linked to cardiovascular diseases, hypertension, and cancer progression, where it may act as a tumor suppressor or promoter depending on context. In cancer, RGS5 is implicated in angiogenesis and tumor stroma remodeling, making it a potential therapeutic target. Recombinant RGS5 serves as a vital tool for *in vitro* assays, including binding studies, enzymatic activity measurements, and drug discovery platforms aimed at modulating GPCR signaling. Its application extends to structural biology for mapping interaction interfaces and developing targeted inhibitors or stabilizers of RGS5 function.
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