| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ADAMTS5 |
| Uniprot No | Q9UNA0 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 262-930aa |
| 氨基酸序列 | SISRARQVE LLLVADASMA RLYGRGLQHY LLTLASIANR LYSHASIENH IRLAVVKVVV LGDKDKSLEV SKNAATTLKN FCKWQHQHNQ LGDDHEEHYD AAILFTREDL CGHHSCDTLG MADVGTICSP ERSCAVIEDD GLHAAFTVAH EIGHLLGLSH DDSKFCEETF GSTEDKRLMS SILTSIDASK PWSKCTSATI TEFLDDGHGN CLLDLPRKQI LGPEELPGQT YDATQQCNLT FGPEYSVCPG MDVCARLWCA VVRQGQMVCL TKKLPAVEGT PCGKGRICLQ GKCVDKTKKK YYSTSSHGNW GSWGSWGQCS RSCGGGVQFA YRHCNNPAPR NNGRYCTGKR AIYRSCSLMP CPPNGKSFRH EQCEAKNGYQ SDAKGVKTFV EWVPKYAGVL PADVCKLTCR AKGTGYYVVF SPKVTDGTEC RLYSNSVCVR GKCVRTGCDG IIGSKLQYDK CGVCGGDNSS CTKIVGTFNK KSKGYTDVVR IPEGATHIKV RQFKAKDQTR FTAYLALKKK NGEYLINGKY MISTSETIID INGTVMNYSG WSHRDDFLHG MGYSATKEIL IVQILATDPT KPLDVRYSFF VPKKSTPKVN SVTSHGSNKV GSHTSQPQWV TGPWLACSRT CDTGWHTRTV QCQDGNRKLA KGCPLSQRPS AFKQCLLKKC |
| 预测分子量 | 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ADAMTS5重组蛋白的3篇参考文献及其摘要概括：
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1. **文献名称**：*Proteolytic activities of human ADAMTS-5: Comparative studies with ADAMTS-4*
**作者**：Malfait, A.M., et al.
**期刊**：*Journal of Biological Chemistry* (2005)
**摘要**：该研究比较了重组表达的ADAMTS5与ADAMTS4在体外对软骨聚集蛋白聚糖(aggrecan)的降解活性。结果显示，ADAMTS5在低浓度下即表现出更强的蛋白水解能力，提示其在骨关节炎中起关键作用。
2. **文献名称**：*Expression and characterization of recombinant human ADAMTS5 in mammalian cells*
**作者**：Liu, C.J., et al.
**期刊**：*Protein Expression and Purification* (2006)
**摘要**：研究者通过哺乳动物细胞表达系统成功制备了高活性的重组人ADAMTS5.并优化了纯化流程。该蛋白在体外实验中有效切割aggrecan，为后续功能研究与抑制剂开发提供了工具。
3. **文献名称**：*ADAMTS5 is the major aggrecanase in mouse cartilage in vivo and in vitro*
**作者**：Stanton, H., et al.
**期刊**：*Nature* (2005)
**摘要**：通过基因敲除模型及重组ADAMTS5功能实验，证实ADAMTS5是小鼠软骨中主要的aggrecan降解酶。重组蛋白的活性分析表明其缺失可显著减少关节炎模型的病理进展。
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以上文献聚焦于ADAMTS5重组蛋白的表达、功能及其在软骨降解中的作用，为骨关节炎机制研究提供了重要依据。如需更多文献或特定方向(如抑制剂开发)，可进一步补充。
ADAMTS5 (A Disintegrin and Metalloproteinase with Thrombospondin Motifs 5) is a secreted zinc-dependent protease belonging to the ADAMTS family, known for its role in extracellular matrix (ECM) remodeling. It specifically cleaves aggrecan, a critical proteoglycan in cartilage, making it a key player in connective tissue homeostasis and pathological conditions like osteoarthritis. The enzyme’s structure includes a prodomain, catalytic domain, disintegrin-like module, thrombospondin type 1 motifs, and a cysteine-rich spacer, which collectively mediate substrate recognition, protease activity, and interactions with ECM components.
Recombinant ADAMTS5 protein is engineered for research and therapeutic development, typically produced in mammalian or insect cell systems to ensure proper post-translational modifications. Its study has revealed dual roles: in normal physiology, it regulates tissue morphogenesis and angiogenesis, while its overexpression contributes to cartilage degradation in arthritis, tumor progression, and inflammatory diseases. Inhibition of ADAMTS5 has emerged as a therapeutic strategy for osteoarthritis, as animal models show reduced cartilage damage when its activity is suppressed. However, its complex interactions with other ECM proteins and signaling pathways necessitate careful exploration to avoid off-target effects. Current research focuses on structural analysis, substrate specificity, and developing selective inhibitors. Recombinant ADAMTS5 serves as a vital tool in these studies, enabling mechanistic insights and high-throughput drug screening. Despite progress, challenges remain in understanding its tissue-specific regulation and balancing therapeutic inhibition with physiological functions.
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