| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | TIMP3 |
| Uniprot No | P35625 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 30-208aa |
| 氨基酸序列 | HPQDAFCNSDIVIRAKVVGKKLVKEGPFGTLVYTIKQMKMYRGFTKMPHVQYIHTEASESLCGLKLEVNKYQYLLTGRVYDGKMYTGLCNFVERWDQLTLSQRKGLNYRYHLGCNCKIKSCYYLPCFVTSKNECLWTDMLSNFGYPGYQSKHYACIRQKGGYCSWYRGWAPPDKSIINA |
| 预测分子量 | 24.8kDa |
| 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TIMP3重组蛋白的3篇参考文献示例(注：内容基于领域内常见研究方向概括，具体文献需通过数据库验证)：
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1. **文献名称**: *Recombinant TIMP-3 inhibits angiogenesis and tumor growth in a preclinical model*
**作者**: Smith et al.
**摘要**: 研究报道了通过哺乳动物细胞表达系统制备重组TIMP3蛋白，并验证其抑制基质金属蛋白酶(MMPs)的活性。实验表明，重组TIMP3通过阻断VEGF信号通路抑制体内血管生成，显著延缓小鼠肿瘤模型中的肿瘤生长。
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2. **文献名称**: *TIMP3 overexpression protects against cardiac fibrosis via MMP inhibition*
**作者**: Chen & Wang
**摘要**: 作者利用重组TIMP3蛋白治疗心肌纤维化模型，发现其通过抑制MMP-2/9活性减少胶原沉积，改善心脏功能。研究强调重组TIMP3在治疗纤维化疾病中的潜在应用。
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3. **文献名称**: *Expression and purification of bioactive human TIMP3 in Escherichia coli*
**作者**: Gupta et al.
**摘要**: 该文献优化了在大肠杆菌中高效表达可溶性重组TIMP3的工艺，通过亲和层析纯化获得高纯度蛋白，并验证其对MMP-3和MMP-9的抑制活性，为大规模生产提供方法学支持。
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**建议**：以上为模拟概括，实际文献请通过PubMed或Google Scholar检索关键词“Recombinant TIMP3 protein”或“TIMP3 overexpression”获取最新信息。
**Background of TIMP3 Recombinant Protein**
Tissue Inhibitor of Metalloproteinases 3 (TIMP3) is a member of the TIMP family, comprising four isoforms (TIMP1–4), which regulate extracellular matrix (ECM) remodeling by inhibiting matrix metalloproteinases (MMPs), ADAMs (a disintegrin and metalloproteinase), and ADAMTSs (ADAM with thrombospondin motifs). Unlike other TIMPs, TIMP3 is tightly bound to the ECM via heparan sulfate proteoglycans, enabling localized control of proteolytic activity. It plays critical roles in maintaining tissue homeostasis, angiogenesis, inflammation, and apoptosis.
Dysregulation of TIMP3 is linked to pathologies such as fibrosis, cancer metastasis, cardiovascular diseases, and age-related macular degeneration (AMD). For instance, reduced TIMP3 expression enhances MMP activity, promoting ECM degradation and tumor invasion, while excessive TIMP3 may impair tissue repair. Genetic mutations in *TIMP3* are associated with Sorsby fundus dystrophy, a rare inherited retinal disorder.
Recombinant TIMP3 protein is produced using expression systems (e.g., bacterial, mammalian) to ensure proper folding and post-translational modifications. It serves as a research tool to study MMP-mediated pathways and a therapeutic candidate for diseases involving ECM imbalance. Preclinical studies highlight its potential in suppressing neovascularization in AMD, mitigating cardiac fibrosis, and inhibiting tumor progression. However, challenges remain in optimizing delivery methods and balancing its dual roles in tissue protection versus pathological ECM stiffening.
Overall, TIMP3 recombinant protein bridges fundamental research and therapeutic innovation, offering insights into ECM dynamics and targeted intervention strategies.
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