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| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IL-36γ |
| Uniprot No | Q9NZH8 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-169aa |
| 氨基酸序列 | MRGTPGDADG GGRAVYQSMC KPITGTINDL NQQVWTLQGQ NLVAVPRSDS VTPVTVAVIT CKYPEALEQG RGDPIYLGIQ NPEMCLYCEK VGEQPTLQLK EQKIMDLYGQ PEPVKPFLFY RAKTGRTSTL ESVAFPDWFI ASSKRDQPII LTSELGKSYN TAFELNIND |
| 预测分子量 | 18.7 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IL-36重组蛋白的3篇参考文献及其摘要概括：
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1. **"Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis"**
*Authors: Marrakchi S, et al. (2011)*
摘要：首次发现IL-36受体拮抗剂(IL-36Ra)基因突变与泛发性脓疱型银屑病(GPP)的关联，研究通过重组蛋白实验表明IL-36信号过度激活驱动皮肤炎症反应。
2. **"IL-36 cytokines in inflammatory and systemic diseases"**
*Authors: Carrier Y, et al. (2015)*
摘要：综述IL-36α/β/γ重组蛋白在炎症性疾病(如银屑病、关节炎)中的作用机制，强调其通过激活NF-κB通路促进促炎因子释放，并探讨治疗靶点潜力。
3. **"IL-36 promotes neutrophil extracellular trap formation and pulmonary neutrophilia in murine psoriasis-like inflammation"**
*Authors: Bridgewood C, et al. (2019)*
摘要：在小鼠银屑病模型中，重组IL-36γ蛋白诱导中性粒细胞胞外陷阱(NETs)形成，证实IL-36直接参与皮肤-肺部炎症轴，为跨器官炎症机制提供证据。
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以上文献涵盖疾病关联、分子机制及治疗应用方向，均为IL-36重组蛋白研究的关键论文。
Interleukin-36 gamma (IL-36γ), a member of the IL-1 cytokine superfamily, is a pro-inflammatory mediator primarily involved in regulating immune responses and inflammatory processes. It is predominantly expressed in epithelial tissues, such as skin, lungs, and intestines, where it plays a critical role in host defense and barrier immunity. IL-36γ signals through a receptor complex comprising IL-36R (IL-1RL2) and IL-1RAcP, activating downstream NF-κB and MAPK pathways to induce the production of chemokines, cytokines, and antimicrobial peptides. Dysregulated IL-36γ signaling has been implicated in chronic inflammatory diseases, including psoriasis, inflammatory bowel disease (IBD), and rheumatoid arthritis.
Recombinant IL-36γ protein is engineered using expression systems like *E. coli* or mammalian cells to produce bioactive forms for research and therapeutic development. The recombinant form typically retains the native structure and function, enabling studies on its role in immune cell activation (e.g., dendritic cells, T cells) and tissue inflammation. Researchers utilize IL-36γ recombinant protein to model inflammatory pathways *in vitro* or *in vivo*, screen potential inhibitors, and explore its therapeutic targeting. For instance, IL-36R antagonists are under clinical investigation for psoriasis treatment, highlighting the cytokine's translational relevance. Its role in amplifying Th17-driven inflammation further underscores its potential as a biomarker or drug target in autoimmune and hyperinflammatory conditions. Despite its pathogenic associations, IL-36γ also contributes to antimicrobial defense, reflecting its dual role in immunity. Ongoing studies aim to unravel context-dependent mechanisms and optimize therapeutic strategies modulating IL-36γ activity.
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