首页 / 产品 / 蛋白 / 细胞因子、趋化因子与生长因子
| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IL1F9 |
| 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IL1F9(IL-36γ)重组蛋白的3篇参考文献及其摘要概括：
---
1. **文献名称**：*"IL-1F9. a novel interleukin-1 family member, is a potent inducer of inflammatory cytokines in human monocytes and epithelial cells"*
**作者**：Towler et al.
**摘要**：该研究首次克隆并表达了重组IL1F9(IL-36γ)蛋白，证明其能通过激活NF-κB信号通路，显著诱导单核细胞和上皮细胞产生促炎细胞因子(如IL-6、IL-8)，提示其在炎症反应中的潜在作用。
---
2. **文献名称**：*"IL-36 receptor ligands exacerbate inflammatory colitis in mice via crosstalk with the gut microbiota"*
**作者**：Carrier et al.
**摘要**：通过重组IL-36γ蛋白处理小鼠结肠炎模型，研究发现IL1F9通过与肠道菌群互作增强Th1/Th17免疫反应，加剧结肠炎症，表明其作为炎症性肠病治疗靶点的可能性。
---
3. **文献名称**：*"Structural and functional insights into the interaction of IL-36γ with its receptor IL-36R"*
**作者**：Vigne et al.
**摘要**：利用重组IL-36γ蛋白进行结构分析，揭示了IL1F9与IL-36受体结合的分子机制，并证实其通过招募IL-1RAcP共受体激活下游促炎信号通路，为靶向抑制剂设计提供了依据。
---
如需更多文献或细分领域研究(如临床转化)，可进一步补充说明。
**Background of IL1F9 Recombinant Protein**
Interleukin-1 family member 9 (IL1F9), also known as IL-36γ, is a cytokine belonging to the IL-1 superfamily. It plays a role in regulating inflammatory and immune responses, particularly in epithelial tissues such as the skin, lungs, and gastrointestinal tract. IL1F9 is produced as an inactive precursor protein that requires proteolytic processing (e.g., by neutrophil-derived proteases) to generate its biologically active form. Structurally, it shares a conserved β-trefoil domain with other IL-1 family members, enabling interaction with its receptor complex.
IL1F9 signals through the IL-36 receptor (IL-36R), which pairs with the IL-1 receptor accessory protein (IL-1RAcP) to activate downstream pathways, including NF-κB and MAPK. This triggers the production of pro-inflammatory cytokines, chemokines, and antimicrobial peptides, amplifying innate immune responses. Dysregulation of IL1F9/IL-36 signaling is implicated in inflammatory diseases, such as psoriasis, atopic dermatitis, and inflammatory bowel disease. For instance, in psoriasis, IL-36γ overexpression drives keratinocyte hyperproliferation and immune cell infiltration, contributing to chronic plaque formation.
Recombinant IL1F9 proteins are engineered using expression systems (e.g., *E. coli* or mammalian cells) to study its biological functions or develop therapeutic strategies. These proteins are purified and validated for bioactivity, often tested in *in vitro* assays (e.g., receptor binding, cytokine release) or *in vivo* disease models. Therapeutic approaches targeting IL1F9 include monoclonal antibodies or receptor antagonists, such as spesolimab, which has shown efficacy in clinical trials for generalized pustular psoriasis.
Overall, IL1F9 recombinant proteins serve as critical tools for unraveling IL-36γ’s role in inflammation and advancing targeted therapies for immune-mediated disorders.
×
