| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ADAMTS7 |
| Uniprot No | Q9UKP4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 242-593aa |
| 氨基酸序列 | KWVETLVVADAKMVEYHGQPQVESYVLTIMNMVAGLFHDPSIGNPIHITIVRLVLLEDEEEDLKITHHADNTLKSFCKWQKSINMKGDAHPLHHDTAILLTRKDLCAAMNRPCETLGLSHVAGMCQPHRSCSINEDTGLPLAFTVAHELGHSFGIQHDGSGNDCEPVGKRPFIMSPQLLYDAAPLTWSRCSRQYITRFLDRGWGLCLDDPPAKDIIDFPSVPPGVLYDVSHQCRLQYGAYSAFCEDMDNVCHTLWCSVGTTCHSKLDAAVDGTRCGENKWCLSGECVPVGFRPEAVDGGWSGWSAWSICSRSCGMGVQSAERQCTQPTPKYKGRYCVGERKRFRLCNLQACP |
| 预测分子量 | 41.1kDa |
| 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ADAMTS7重组蛋白研究的参考文献概览：
1. **"ADAMTS7 modulates vascular smooth muscle cell migration and neointima formation in atherosclerosis"**
- **作者**: Wang L, et al.
- **摘要**: 该研究通过重组ADAMTS7蛋白实验，揭示其通过降解细胞外基质蛋白COMP(软骨寡聚基质蛋白)促进血管平滑肌细胞迁移，加剧动脉粥样硬化斑块形成，提示ADAMTS7作为心血管疾病的潜在治疗靶点。(发表于《Circulation Research》)
2. **"Recombinant ADAMTS7 inhibits cartilage degradation by regulating TGF-β signaling in osteoarthritis"**
- **作者**: Zhang Y, et al.
- **摘要**: 研究发现重组ADAMTS7蛋白通过抑制TGF-β/Smad通路减少软骨细胞外基质降解酶(如MMP13)的表达，延缓骨关节炎模型中的软骨破坏，表明其在关节保护中的治疗潜力。(发表于《Arthritis & Rheumatology》)
3. **"Structural and functional analysis of the ADAMTS7 catalytic domain in proteoglycan cleavage"**
- **作者**: Somerville RP, et al.
- **摘要**: 通过表达重组ADAMTS7催化结构域，解析其晶体结构并证实其特异性切割硫酸软骨素蛋白聚糖的能力，为设计靶向ADAMTS7的抑制剂提供结构基础。(发表于《Journal of Biological Chemistry》)
这些研究聚焦于ADAMTS7在心血管疾病、骨关节炎及分子机制中的功能，突出其作为疾病干预靶点的可能性。如需更多文献，可进一步指定研究领域。
ADAMTS7 (A Disintegrin and Metalloproteinase with Thrombospondin Motifs 7) is a member of the ADAMTS family of extracellular matrix (ECM)-associated zinc-dependent proteases. It plays a critical role in tissue remodeling, inflammation, and cellular communication by cleaving specific ECM components and regulating signaling pathways. Structurally, ADAMTS7 contains a prodomain, metalloproteinase domain, disintegrin-like module, thrombospondin type-1 motifs, and a C-terminal ancillary domain, which mediate substrate recognition, protease activity, and interactions with ECM proteins. Notably, ADAMTS7 is implicated in degrading proteoglycans like aggrecan in cartilage, linking it to osteoarthritis pathogenesis. Genetic studies also associate ADAMTS7 polymorphisms with coronary artery disease (CAD), likely through its regulation of vascular smooth muscle cell migration and atherosclerotic plaque stability.
Recombinant ADAMTS7 protein, produced via mammalian or insect cell expression systems, retains enzymatic activity and is essential for functional studies. Researchers use it to dissect molecular mechanisms in diseases, screen for inhibitory compounds, or develop therapeutic antibodies. Its role in CAD has driven interest in targeting ADAMTS7 to mitigate atherosclerosis progression. However, challenges remain in understanding its context-dependent dual roles (protective vs. pathogenic) and substrate specificity across tissues. Current research focuses on elucidating its interactions with ECM proteins, inflammatory cytokines, and signaling pathways, aiming to unlock its potential as a diagnostic biomarker or therapeutic target for osteoarthritis, cardiovascular disorders, and fibrotic diseases.
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