| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SIKE1 |
| Uniprot No | Q9BRV8 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-207aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMSCTIEK ILTDAKTLLE RLREHDAAAE SLVDQSAALH RRVAAMREAG TALPDQYQED ASDMKDMSKY KPHILLSQEN TQIRDLQQEN RELWISLEEH QDALELIMSK YRKQMLQLMV AKKAVDAEPV LKAHQSHSAE IESQIDRICE MGEVMRKAVQ VDDDQFCKIQ EKLAQLELEN KELRELLSIS SESLQARKEN SMDTASQAIK |
| 预测分子量 | 26 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SIKE1重组蛋白的3篇参考文献的简要信息(注：文献为模拟示例，实际引用需核实)：
1. **文献名称**：*Molecular characterization of SIKE1 as an innate immune suppressor*
**作者**：Smith A, et al.
**摘要**：本研究成功构建了重组SIKE1蛋白，验证其通过抑制IKKε-TBK1信号通路负调控干扰素产生，并解析了其与下游激酶的相互作用机制。
2. **文献名称**：*Expression and functional analysis of recombinant SIKE1 in antiviral responses*
**作者**：Zhang L, et al.
**摘要**：报道了在大肠杆菌中高效表达可溶性SIKE1重组蛋白的方法，证实其通过阻断RIG-I信号通路抑制病毒诱导的I型干扰素表达。
3. **文献名称**：*Structural insights into SIKE1-mediated immune regulation*
**作者**：Wang Y, et al.
**摘要**：利用重组SIKE1蛋白进行晶体结构解析，揭示了其C端结构域与IKKε激酶的结合界面，为设计靶向免疫调节药物提供结构基础。
(注：实际研究中SIKE1相关文献较少，建议通过PubMed/Google Scholar以关键词"SIKE1 recombinant"+"IKKε"检索最新进展。)
SIKE1 (Suppressor of IKKε 1) is an adapter protein implicated in innate immune signaling pathways, particularly those regulating interferon (IFN) production. It was initially identified as a negative regulator of IKKε (Inhibitor of Nuclear Factor Kappa-B Kinase Subunit Epsilon) and TBK1 (TANK-Binding Kinase 1), key kinases involved in antiviral responses. Structurally, SIKE1 contains a conserved SKICH (SKIP C-terminal Homology) domain, which facilitates protein-protein interactions critical for its regulatory function.
In the context of viral infection, SIKE1 binds to IKKε/TBK1. disrupting their interaction with downstream adaptors like MAVS or STING, thereby suppressing the phosphorylation and activation of IRF3/7 transcription factors required for type I IFN production. This modulation helps balance immune activation to prevent excessive inflammation. However, SIKE1's activity appears cell type-specific; it is highly expressed in immune cells but shows variable regulation in other tissues.
Beyond antiviral immunity, SIKE1 interacts with cytoskeletal proteins such as α-actinin, suggesting roles in cell motility and structural organization. Dysregulation of SIKE1 has been linked to autoimmune diseases and cancer progression, where its tumor-suppressive or oncogenic effects may depend on cellular context. For example, reduced SIKE1 expression correlates with enhanced IFN signaling in lupus models, while its overexpression in certain cancers inhibits metastasis.
Recombinant SIKE1 protein is commonly produced in E. coli or mammalian systems for functional studies, enabling researchers to dissect its mechanistic roles in immune regulation and disease pathogenesis. Its therapeutic potential as a modulator of IFN pathways continues to be explored in inflammatory disorders and antiviral therapies.
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