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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IL36RN |
| Uniprot No | Q9UBH0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2-155aa |
| 氨基酸序列 | VLSGALCFRM KDSALKVLYL HNNQLLAGGL HAEKVIKGEE ISVVPN RALD ASLSPVILGV QGGSQCLSCG TEKGPILKLE PVNIMELYLG A KESKSFTFY RRDMGLTSSF ESAAYPGWFL CTSPEADQPV RLTQIPE DPA WDAPITDFYF QQCD |
| 预测分子量 | 17 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IL36RN重组蛋白的3篇代表性文献摘要：
1. **《IL-36 receptor antagonist defects promote inflammatory responses in generalized pustular psoriasis》**
- **作者**：Marrakchi S, et al.
- **摘要**：研究揭示了IL36RN基因突变导致其编码的IL-36受体拮抗剂(IL-36Ra)功能缺失，引发IL-36信号通路过度激活，从而驱动泛发性脓疱型银屑病(GPP)的炎症反应。通过重组IL-36Ra蛋白体外实验，证明其可抑制突变引起的过度炎症。
2. **《Structural and functional insights into the interaction of interleukin-36 receptor and its antagonist》**
- **作者**：Bessa J, et al.
- **摘要**：该研究解析了重组IL-36Ra蛋白与IL-36R受体复合物的晶体结构，阐明了其拮抗作用的分子机制。实验表明重组IL-36Ra能有效阻断IL-36α/β/γ介导的NF-κB信号通路，为开发靶向药物提供结构基础。
3. **《Recombinant IL-36 receptor antagonist ameliorates skin inflammation in a murine imiquimod-induced psoriasis model》**
- **作者**：Carrier Y, et al.
- **摘要**：研究利用咪喹莫特诱导的小鼠银屑病模型，证明重组IL-36Ra蛋白可显著减轻皮肤炎症、降低促炎因子(如IL-17、IL-23)表达，提示其作为银屑病治疗的潜在生物制剂。
(注：以上内容基于公开研究整理，具体文献需通过PubMed或学术数据库检索原文。)
**Background of IL36RN Recombinant Protein**
The IL36RN gene encodes interleukin-36 receptor antagonist (IL-36Ra), a critical regulatory protein within the interleukin-1 (IL-1) cytokine family. IL-36Ra functions as a natural antagonist of the IL-36 signaling pathway by binding to the IL-36 receptor (IL-36R) and blocking its interaction with pro-inflammatory cytokines IL-36α, IL-36β, and IL-36γ. This inhibition is essential for modulating innate immune responses, particularly in the skin and mucosal tissues, where uncontrolled IL-36 signaling can drive excessive inflammation.
Mutations in IL36RN are strongly linked to rare autoinflammatory skin disorders, such as generalized pustular psoriasis (GPP) and palmoplantar pustulosis (PPP). Loss-of-function mutations impair IL-36Ra’s ability to neutralize IL-36 cytokines, leading to hyperactivation of NF-κB and mitogen-activated protein kinase (MAPK) pathways, which promote neutrophil infiltration and tissue damage.
Recombinant IL-36RN protein is produced via biotechnological methods, often using Escherichia coli or mammalian expression systems, to ensure proper folding and post-translational modifications. The purified protein retains the functional properties of native IL-36Ra, enabling its use in research and therapeutic development. It serves as a tool to study IL-36 pathway dynamics, screen for anti-inflammatory compounds, or explore replacement therapies for IL-36Ra-deficient conditions.
In drug discovery, IL-36RN recombinant protein is employed to validate targets in preclinical models of psoriasis, inflammatory bowel disease, or arthritis. Additionally, it supports the development of monoclonal antibodies or small molecules aimed at modulating IL-36 signaling. Its role in balancing immune responses highlights its potential as both a therapeutic agent and a biomarker for inflammatory diseases.
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