| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | Smad7 |
| Uniprot No | O15105 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 160-260aa |
| 氨基酸序列 | CKVFRWPDLRHSSEVKRLCCCESYGKINPELVCCNPHHLSRLCELESPPP PYSRYPMDFLKPTADCPDAVPSSAETGGTNYLAPGGLSDSQLLLEPGDRS H |
| 预测分子量 | 37 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篇关于Smad7重组蛋白的文献信息(文献名称、作者及摘要概括)：
1. **"Smad7重组蛋白通过抑制TGF-β/Smad通路减轻肝纤维化"**
*作者：Yan X, Zhang L, et al. (2015)*
摘要：研究证明，体外表达的Smad7重组蛋白可通过阻断TGF-β1介导的Smad2/3磷酸化，抑制肝星状细胞活化，显著改善小鼠肝纤维化模型中的胶原沉积。
2. **"重组Smad7蛋白抑制炎症性肠病中的异常免疫反应"**
*作者：Monteleone G, Boirivant M, et al. (2004)*
摘要：通过动物实验发现，肠道局部递送Smad7重组蛋白可阻断TGF-β信号传导，减少促炎细胞因子(如TNF-α、IL-6)的产生，缓解结肠炎症损伤。
3. **"外源性Smad7重组蛋白增强化疗药物对胰腺癌细胞的敏感性"**
*作者：Kim SG, Park K, et al. (2010)*
摘要：体外实验表明，Smad7重组蛋白通过拮抗TGF-β介导的EMT(上皮间质转化)过程，逆转肿瘤细胞耐药性，显著提高吉西他滨的细胞毒性作用。
4. **"Smad7重组蛋白在糖尿病肾病中的保护机制研究"**
*作者：Meng XM, Huang XR, et al. (2013)*
摘要：研究显示，静脉注射Smad7重组蛋白可抑制肾小球系膜细胞纤维化标志物(如α-SMA、纤连蛋白)表达，延缓糖尿病小鼠肾脏病变进展。
注：以上文献标题和作者为示例性内容，实际文献需通过PubMed或Web of Science以具体关键词检索。建议优先选择《Nature Communications》《Journal of Biological Chemistry》等期刊近五年内的高被引论文。
Smad7 is a key regulatory protein within the transforming growth factor-beta (TGF-β) signaling pathway, which plays critical roles in cell proliferation, differentiation, apoptosis, and immune responses. As an inhibitory Smad (I-Smad), Smad7 antagonizes the activation of receptor-regulated Smads (R-Smads, e.g., Smad2/3) by blocking their phosphorylation through competitive binding to activated TGF-β type I receptors. This negative feedback mechanism ensures tight control over TGF-β signaling, preventing excessive cellular responses linked to fibrosis, cancer progression, and chronic inflammation.
Recombinant Smad7 protein is engineered using expression systems (e.g., E. coli, mammalian, or insect cells) to produce purified, bioactive forms of the protein for research and therapeutic applications. Its structure typically retains functional domains, including the MH2 domain essential for receptor interaction. Researchers utilize recombinant Smad7 to study TGF-β pathway modulation, particularly in diseases where dysregulated signaling contributes to pathology, such as renal fibrosis, inflammatory bowel disease, and metastatic cancers. In preclinical studies, exogenous Smad7 delivery has shown potential in suppressing TGF-β-driven epithelial-mesenchymal transition (EMT) and collagen deposition.
Additionally, Smad7 recombinant protein serves as a tool for drug discovery, enabling high-throughput screening of molecules that mimic or enhance its inhibitory effects. Challenges in its application include optimizing delivery methods (e.g., viral vectors or nanoparticles) and ensuring stability in physiological environments. Ongoing research focuses on harnessing Smad7's therapeutic potential while balancing its dual role, as prolonged inhibition may inadvertently disrupt homeostatic TGF-β functions in tissue repair and immunity.
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