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| 纯度 | >95%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IL35 |
| Uniprot No | P29459 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 23-219aa |
| 氨基酸序列 | RNLPVATPDPGMFPCLHHSQNLLRAVSNMLQKARQTLEFYPCTSEEIDHE DITKDKTSTVEACLPLELTKNESCLNSRETSFITNGSCLASRKTSFMMAL CLSSIYEDLKMYQVEFKTMNAKLLMDPKRQIFLDQNMLAVIDELMQALNF NSETVPQKSSLEEPDFYKTKIKLCILLHAFRIRAVTIDRVMSYLNAS |
| 预测分子量 | 25 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3-4条关于IL35重组蛋白的模拟参考文献(部分内容基于真实研究概括，但文献名称和作者为虚构示例)：
1. **《IL-35 recombinant protein suppresses autoimmune inflammation via regulatory B cells》**
- 作者：Smith A, et al.
- 摘要：研究利用哺乳动物细胞表达的IL35重组蛋白，证明其通过激活调节性B细胞(Bregs)抑制小鼠实验性自身免疫性脑脊髓炎(EAE)的炎症反应，揭示IL35在自身免疫疾病治疗中的潜在机制。
2. **《Production and functional characterization of human IL-35 in a prokaryotic expression system》**
- 作者：Li X, et al.
- 摘要：开发了大肠杆菌表达系统生产重组人IL35蛋白的方法，验证其与天然IL35相似的免疫抑制功能，并证实其通过STAT1/STAT3信号通路抑制Th17细胞分化。
3. **《IL-35 recombinant protein alleviates colitis by expanding T regulatory cells》**
- 作者：Wang Y, et al.
- 摘要：在小鼠结肠炎模型中，注射IL35重组蛋白显著减轻肠道炎症，其机制与诱导Treg细胞扩增及抑制促炎因子IL-17和IFN-γ分泌相关。
4. **《Structural insights into IL-35 heterodimer formation and receptor binding》**
- 作者：Johnson R, et al.
- 摘要：通过晶体学分析重组IL35(IL12A-EBI3异源二聚体)的结构，揭示其与受体IL12Rβ2和gp130的结合模式，为设计靶向IL35的免疫调节药物提供理论依据。
(注：以上文献为示例性质，实际引用时需以真实发表的论文为准。)
Interleukin-35 (IL-35), a member of the interleukin-12 (IL-12) cytokine family, is an immunosuppressive heterodimeric protein composed of Epstein-Barr virus-induced gene 3 (EBI3) and interleukin-12 alpha (IL-12α/p35) subunits. First identified in 2007 as a product of regulatory T cells (Tregs), IL-35 distinguishes itself from other IL-12 family cytokines by its unique role in immune suppression. It is primarily secreted by Tregs and certain B cells (Bregs) to mediate tolerance and limit excessive inflammatory responses. Structurally, IL-35 requires the pairing of EBI3 and p35 subunits, which form a functional heterodimer through disulfide bonds. Unlike IL-12 or IL-23. IL-35 signals through a distinct receptor complex involving IL-12Rβ2 and gp130 subunits, activating STAT1/STAT4 pathways in T cells to promote immunosuppression.
Biologically, IL-35 suppresses effector T cell proliferation, induces the conversion of conventional T cells into regulatory phenotypes (iTreg35), and inhibits pro-inflammatory cytokine production. Its immunosuppressive functions are implicated in autoimmune diseases, cancer, and chronic infections. For instance, elevated IL-35 levels correlate with tumor progression by fostering an immune-tolerant microenvironment, while its deficiency exacerbates autoimmune conditions like colitis or rheumatoid arthritis.
Recombinant IL-35 protein is produced using mammalian expression systems (e.g., HEK293 or CHO cells) to ensure proper post-translational modifications. Purification typically involves affinity chromatography tags (e.g., His-tag) fused to one subunit. Research applications include studying immune tolerance mechanisms, developing therapeutic strategies for autoimmune disorders, and exploring its dual roles in cancer immunotherapy. However, challenges remain in understanding context-dependent functions and optimizing clinical applications due to its pleiotropic effects.
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