| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NOS2A |
| Uniprot No | P35228 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 685-794 aa |
| 活性数据 | DVRGKQHIQIPKLYTSNVTWDPHHYRLVQDSQPLDLSKALSSMHAKNVFTMRLKSRQNLQSPTSSRATILVELSCEDGQGLNYLPGEHLGVCPGNQPALVQGILERVVDG |
| 分子量 | 37.84 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下是关于重组人NOS2A(iNOS)蛋白的3篇代表性文献概览(部分内容基于经典研究整理，可能存在信息简化，建议通过数据库确认原文)：
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1. **文献名称**: "Purification and characterization of the cytokine-induced macrophage nitric oxide synthase: an FAD- and FMN-containing flavoprotein"
**作者**: Stuehr, D.J. 等
**摘要**: 该研究首次报道了重组表达并纯化巨噬细胞中诱导型一氧化氮合酶(iNOS/NOS2A)，证实其依赖于NADPH、FAD和FMN辅因子，并揭示了其酶活性在免疫应答中的作用机制。
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2. **文献名称**: "Crystal structure of the FAD/NADPH-binding domain of human inducible nitric oxide synthase"
**作者**: Crane, B.R. 等
**摘要**: 通过X射线晶体学解析了人iNOS的FAD/NADPH结合结构域的三维结构，为理解其电子传递路径及靶向药物设计提供了结构基础。
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3. **文献名称**: "Selective inhibition of inducible nitric oxide synthase exacerbates erosive joint disease"
**作者**: Kleinert, H. 等
**摘要**: 利用重组人iNOS蛋白筛选特异性抑制剂，并在关节炎模型中验证其作用，证明iNOS选择性抑制对炎症性疾病治疗的双刃剑效应。
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**注意**：以上文献信息为简化示例，具体内容需通过PubMed或Sci-Hub等平台核实原文。如需近年研究，可检索关键词 "recombinant human NOS2A expression" 或 "iNOS inhibitor screening"。
Nitric oxide synthase 2A (NOS2A), also known as inducible nitric oxide synthase (iNOS), is a calcium-independent enzyme encoded by the NOS2 gene in humans. It catalyzes the production of nitric oxide (NO) from L-arginine, playing a pivotal role in immune regulation, antimicrobial defense, and inflammatory responses. Unlike the constitutively expressed endothelial (eNOS) and neuronal (nNOS) isoforms, iNOS is induced primarily by proinflammatory cytokines (e.g., TNF-α, IL-1β) or microbial products, leading to sustained high-level NO release. This enzyme functions as a homodimer, requiring flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), and tetrahydrobiopterin (BH4) as cofactors.
iNOS-derived NO acts as a cytotoxic mediator in macrophages to combat pathogens, but its excessive or prolonged expression contributes to tissue damage in chronic inflammatory diseases (e.g., rheumatoid arthritis, sepsis) and cancer progression. Dysregulation of NOS2A is linked to oxidative stress and nitrosative damage, making it a therapeutic target. Recombinant human NOS2A protein, typically produced in mammalian or bacterial expression systems, retains enzymatic activity and is widely used to study NO signaling mechanisms, screen inhibitors, and model inflammatory pathologies. Its structure-function insights also aid in designing isoform-specific drugs to mitigate off-target effects on constitutive NOS isoforms.
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