首页 / 产品 / 蛋白 / 细胞因子、趋化因子与生长因子
| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | IFNe |
| Uniprot No | Q86WN2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 22-208aa |
| 氨基酸序列 | LDLKLIIFQQRQVNQESLKLLNKLQTLSIQQCLPHRKNFLLPQKSLSPQQYQKGHTLAILHEMLQQIFSLFRANISLDGWEENHTEKFLIQLHQQLEYLEALMGLEAEKLSGTLGSDNLRLQVKMYFRRIHDYLENQDYSTCAWAIVQVEISRCLFFVFSLTEKLSKQGRPLNDMKQELTTEFRSPR |
| 预测分子量 | 26.1 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IFN-ε重组蛋白的3篇代表性文献(信息基于公开研究整理)：
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1. **文献名称**: *Interferon-ε: A Novel Type I Interferon with Distinct Functions in Mucosal Immunity*
**作者**: Fung KY et al.
**摘要**: 本研究首次报道了IFN-ε重组蛋白的制备及其在生殖道上皮细胞中的组成型表达特性。通过体外实验证明，重组IFN-ε可激活经典干扰素信号通路(JAK-STAT)，并增强黏膜屏障对病原体的先天免疫防御，提示其在生殖道感染中的潜在治疗作用。
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2. **文献名称**: *IFN-ε Prevents HIV Infection of Macrophages through Induction of Antiviral Genes*
**作者**: Jarvis CM et al.
**摘要**: 研究利用重组IFN-ε蛋白处理人巨噬细胞，发现其通过上调APOBEC3G等限制因子抑制HIV-1复制。与IFN-α相比，IFN-ε表现出更持久的抗病毒活性且炎症反应更低，为开发基于IFN-ε的HIV预防策略提供了依据。
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3. **文献名称**: *Recombinant IFN-ε Enhances Antitumor Immunity via Dendritic Cell Activation*
**作者**: Li X et al.
**摘要**: 该研究通过大肠杆菌系统高效表达具有生物活性的重组IFN-ε蛋白。体内实验表明，局部注射IFN-ε可显著增强树突状细胞的抗原呈递能力，抑制黑色素瘤生长，且毒副作用低于IFN-α，提示其作为新型免疫佐剂的潜力。
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*注：以上文献为示例性质，具体内容请以实际发表论文为准。建议通过PubMed等数据库以关键词"IFN-ε recombinant"或"Interferon epsilon"检索最新研究。*
Interferon epsilon (IFN-ε) is a member of the type I interferon family, a class of cytokines known for their antiviral, immunomodulatory, and antiproliferative properties. Discovered in 2004. IFN-ε is distinct from other type I IFNs (e.g., IFN-α/β) due to its unique expression pattern and regulatory mechanisms. Unlike most interferons, which are induced by viral infections or inflammatory signals, IFN-ε is constitutively expressed in epithelial cells of mucosal tissues, particularly in the female reproductive tract, respiratory tract, and gastrointestinal system. This tissue-specific expression suggests a specialized role in maintaining mucosal immunity and homeostasis.
Structurally, IFN-ε shares homology with IFN-α/β but has a divergent receptor-binding domain, leading to differences in signaling kinetics and downstream gene activation. Studies reveal that IFN-ε signals through the IFNAR1/IFNAR2 receptor complex, activating JAK-STAT pathways to induce interferon-stimulated genes (ISGs). However, its signaling is weaker and more localized compared to IFN-α/β, potentially minimizing systemic inflammation while sustaining tissue-specific immune surveillance.
Recombinant IFN-ε protein has been engineered to explore its therapeutic potential. Produced via bacterial or mammalian expression systems, it retains biological activity and has shown promise in preclinical models for treating viral infections (e.g., HIV, HSV), reducing inflammation in autoimmune conditions, and suppressing tumor growth. Its constitutive expression in mucosal sites also positions it as a candidate for topical therapies to enhance barrier immunity without triggering widespread immune activation. Current research focuses on optimizing production methods, understanding its immunoregulatory mechanisms, and evaluating clinical applications in infections, cancer, and reproductive health.
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