| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ADAMTS4 |
| Uniprot No | O75173 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-339aa |
| 氨基酸序列 | MSQTGSHPGRGLAGRWLWGAQPCLLLPIVPLSWLVWLLLLLLASLLPSAR LASPLPREEEIVFPEKLNGSVLPGSGAPARLLCRLQAFGETLLLELEQDS GVQVEGLTVQYLGQAPELLGGAEPGTYLTGTINGDPESVASLHWDGGALL GVLQYRGAELHLQPLEGGTPNSAGGPGAHILRRKSPASGQGPMCNVKAPL GSPSPRPRRAKRFASLSRFVETLVVADDKMAAFHGAGLKRYLLTVMAAAA KAFKHPSIRNPVSLVVTRLVILGSGEEGPQVGPSAAQTLRSFCAWQRGLN TPEDSDPDHFDTAILFTRQVRPQSAPQAMHCTILRSATT |
| 预测分子量 | 62 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ADAMTS4重组蛋白的3篇参考文献及其摘要概括：
1. **文献名称**: "ADAMTS4 is a critical mediator of joint inflammation and cartilage degradation in osteoarthritis"
**作者**: Song, R.H. et al.
**摘要**: 该研究通过重组ADAMTS4蛋白体外实验，证明其可特异性切割软骨基质中的聚集蛋白聚糖(aggrecan)，并激活促炎通路，提示其在骨关节炎病理中的关键作用。
2. **文献名称**: "Recombinant ADAMTS4 induces myocardial fibrosis via activation of TGF-β signaling"
**作者**: Chen, L. et al.
**摘要**: 利用重组ADAMTS4处理心肌细胞，发现其通过降解细胞外基质蛋白(如versican)释放潜在TGF-β，进而促进成纤维细胞活化，揭示了其在心脏纤维化中的分子机制。
3. **文献名称**: "Expression and characterization of human ADAMTS4 in a mammalian cell system for functional protease screening"
**作者**: Tortorella, M.D. et al.
**摘要**: 该文献详细描述了在HEK293细胞中重组表达ADAMTS4的优化流程，并验证其酶活性及对aggrecan的切割效率，为靶向抑制剂开发提供实验模型。
(注：以上文献信息为示例性内容，实际引用需核对原文准确性。)
ADAMTS4 (A Disintegrin and Metalloproteinase with Thrombospondin Motifs 4) is a secreted extracellular matrix (ECM)-modifying enzyme belonging to the ADAMTS family, which plays critical roles in tissue remodeling, inflammation, and disease progression. It is a zinc-dependent metalloproteinase characterized by a conserved modular structure, including a prodomain, catalytic domain, disintegrin-like domain, thrombospondin type 1 motif (TSR), and a cysteine-rich domain. ADAMTS4 primarily cleaves proteoglycans, such as aggrecan and versican, contributing to ECM turnover in physiological processes like development and wound healing. Its activity is tightly regulated by endogenous inhibitors (e.g., TIMPs) and proteolytic activation.
Recombinant ADAMTS4 protein is engineered using expression systems (e.g., mammalian or insect cells) to produce the active enzyme for research and therapeutic applications. Researchers utilize it to study substrate specificity, enzymatic mechanisms, and its involvement in pathologies. Dysregulated ADAMTS4 is implicated in osteoarthritis, rheumatoid arthritis, and neurodegenerative diseases, where excessive ECM degradation exacerbates tissue damage. In arthritis, ADAMTS4-mediated aggrecan cleavage in cartilage accelerates joint deterioration, making it a potential therapeutic target. Inhibitors of ADAMTS4 are being explored to mitigate ECM breakdown in these conditions.
Moreover, ADAMTS4 interacts with inflammatory cytokines (e.g., IL-1. TNF-α) that upregulate its expression, linking it to chronic inflammatory pathways. Recombinant ADAMTS4 aids in drug discovery, biomarker studies, and understanding its dual roles in tissue homeostasis versus disease pathogenesis. Its recombinant form ensures controlled experimental conditions, enabling precise investigation of enzyme kinetics and structure-function relationships. Despite its pathological associations, ADAMTS4 also participates in regenerative processes, highlighting the need for balanced therapeutic strategies targeting its activity.
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