| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ECRG4 |
| Uniprot No | Q9H1Z8 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 71-132aa |
| 氨基酸序列 | QLWDRTRPEVQQWYQQFLYMGFDEAKFEDDITYWLNRDRNGHEYYGDYYQRHYDEDSAIGPR |
| 预测分子量 | 12.9 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ECRG4重组蛋白的3篇参考文献示例(注：以下内容为模拟生成，非真实文献)：
1. **文献名称**：*"Recombinant ECRG4 inhibits tumor growth by suppressing angiogenesis in esophageal carcinoma"*
**作者**：Li Y, Wang X, Zhang H.
**摘要**：本研究通过在大肠杆菌中表达并纯化重组ECRG4蛋白，发现其能显著抑制食管癌细胞的迁移和血管生成。动物实验表明，ECRG4重组蛋白通过下调VEGF信号通路抑制肿瘤生长。
2. **文献名称**：*"Structural and functional characterization of ECRG4 as a novel tumor suppressor"*
**作者**：Chen L, Liu T, Guo S.
**摘要**：通过X射线晶体学解析了ECRG4重组蛋白的三维结构，揭示了其与细胞表面受体uPAR的相互作用位点。体外实验证实，重组ECCRG4通过诱导细胞周期阻滞抑制多种癌症增殖。
3. **文献名称**：*"ECRG4 recombinant protein modulates innate immune response in sepsis models"*
**作者**：Smith J, Patel R, Brown K.
**摘要**：研究发现，ECRG4重组蛋白可通过TLR4/NF-κB通路抑制过度炎症反应。在脓毒症小鼠模型中，ECRG4显著降低促炎因子水平，提示其作为免疫调节剂的潜力。
如需具体文献，建议通过PubMed或Web of Science以关键词“ECRG4 recombinant protein”检索最新研究。
ECRG4 (Esophageal Cancer-Related Gene 4), initially identified as a candidate tumor suppressor in esophageal squamous cell carcinoma, encodes a secreted protein implicated in diverse cellular processes, including tumorigenesis, inflammation, and immune regulation. The gene, located on human chromosome 2q12. produces a precursor protein of approximately 14 kDa that undergoes proteolytic cleavage to generate bioactive peptides. These peptides exhibit context-dependent functions, acting either as tumor suppressors by inhibiting cell proliferation, migration, and invasion, or as innate immune mediators through interactions with pattern recognition receptors like TLR4.
Epigenetic silencing of ECRG4 via promoter hypermethylation is frequently observed in multiple cancers (e.g., breast, prostate, glioblastoma), correlating with advanced disease and poor prognosis. Its downregulation is associated with enhanced cancer cell survival, angiogenesis, and metastasis. Conversely, recombinant ECRG4 protein—produced via bacterial or mammalian expression systems—has shown therapeutic potential in preclinical models. It suppresses tumor growth by inducing apoptosis, modulating cell cycle arrest, and inhibiting NF-κB signaling.
Beyond oncology, ECRG4 regulates inflammatory responses and tissue homeostasis. It is expressed in epithelial barriers (e.g., skin, gut) and the central nervous system, suggesting roles in mucosal immunity and neuroinflammation. Structural studies reveal its homology to host defense peptides, supporting its dual role in tumor suppression and innate immunity.
Current research focuses on optimizing recombinant ECRG4 for clinical translation, addressing challenges like protein stability, delivery mechanisms, and context-specific signaling effects. Its dual functionality positions it as a promising multifunctional agent for cancer therapy and immune modulation.
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