| 纯度 | >90%SDS-PAGE. |
| 种属 | Mouse |
| 靶点 | Irag1 |
| Uniprot No | Q9WUX5 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 451-550aa |
| 氨基酸序列 | NLVGFKLPELSEAAEQDKGVSPELAPAAEEEESKSGLDVMPNISDILLRKLRVHKSLTGSAPPLTEKEVENVFVQLSLAFRNDSYTLESRINQAERERNL |
| 预测分子量 | 18.5 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IRAG1(Inositol 1.4.5-Triphosphate Receptor-Associated cGMP Kinase Substrate 1)重组蛋白的参考文献摘要及关键信息：
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1. **文献名称**: **"IRAG mediates NO/cGMP-dependent inhibition of platelet aggregation and thrombus formation"**
**作者**: Antl M, et al.
**摘要**: 该研究揭示了IRAG1在血小板中通过NO/cGMP信号通路调控细胞内钙离子释放，从而抑制血小板聚集和血栓形成。通过重组蛋白实验，证明IRAG1与IP3受体相互作用是抑制血小板活化的关键机制。
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2. **文献名称**: **"Regulation of intracellular calcium by a signalling complex of IRAG, IP3 receptor and cGMP kinase Iβ"**
**作者**: Schlossmann J, et al.
**摘要**: 作者利用重组IRAG1蛋白，阐明了其与IP3受体和cGMP激酶Iβ形成复合物的分子机制。研究表明，该复合物通过调控钙离子通道活性影响平滑肌收缩，为心血管疾病治疗提供潜在靶点。
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3. **文献名称**: **"Role of IRAG1 in vascular smooth muscle cell relaxation and blood pressure regulation"**
**作者**: Ammendola A, et al.
**摘要**: 通过重组IRAG1蛋白的功能分析，发现其在血管平滑肌细胞中通过cGMP依赖性途径降低细胞内钙浓度，促进血管舒张，进而参与血压调节。缺失IRAG1的小鼠表现出高血压表型。
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4. **文献名称**: **"Structural and functional characterization of the IRAG1-IP3 receptor interaction"**
**作者**: Huber A, et al.
**摘要**: 该研究利用重组IRAG1蛋白解析了其与IP3受体的结合域结构，揭示了二者相互作用的关键氨基酸位点。功能实验表明，该结合对细胞内钙信号动态平衡至关重要。
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**备注**：IRAG1相关研究多集中于其在钙信号调控和心血管系统中的功能，重组蛋白技术常用于解析其分子机制或开发靶向疗法。如需具体文献来源(期刊、年份等)，建议通过PubMed或Web of Science检索上述标题及作者。
IRAG1 (Inositol 1.4.5-Trisphosphate Receptor-Associated GAP1), also known as MRVI1 (Murine Retrovirus Integration Site 1), is a protein encoded by the *MRVI1* gene in humans. It was initially identified through its association with the type 1 inositol 1.4.5-trisphosphate receptor (IP3R1), a critical calcium release channel in the endoplasmic reticulum. IRAG1 plays a regulatory role in intracellular calcium signaling by forming a complex with IP3R1 and cyclic GMP-dependent protein kinase Iα (PKGIα). This interaction is essential for modulating calcium flux, particularly in vascular smooth muscle cells, where it contributes to nitric oxide (NO)/cGMP-mediated vasorelaxation and blood pressure regulation.
Structurally, IRAG1 contains a conserved GAP1 domain, which is implicated in its interaction with IP3R1. and multiple phosphorylation sites targeted by PKGIα. Studies in knockout mice revealed that IRAG1 deficiency leads to impaired cGMP-dependent inhibition of IP3-induced calcium release, resulting in hypertension and cardiovascular dysfunction. Beyond its role in vascular biology, IRAG1 has been linked to platelet activation, immune responses, and tumor suppression, though these pathways remain less characterized.
Recombinant IRAG1 protein is commonly produced in *E. coli* or mammalian expression systems for biochemical and functional studies. It serves as a tool to investigate calcium signaling mechanisms, screen for modulators of IP3R1 activity, or explore therapeutic strategies targeting hypertension and thrombosis. Its unique position at the intersection of calcium and cGMP signaling continues to make it a subject of interest in cardiovascular and cellular physiology research.
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