| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | ADAMTSL5 |
| Uniprot No | Q6ZMM2 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 43-481aa |
| 氨基酸序列 | QGPGEWTPWVSWTRCSSSCGRGVSVRSRRCLRLPGEEPCWGDSHEYRLCQLPDCPPGAVPFRDLQCALYNGRPVLGTQKTYQWVPFHGAPNQCDLNCLAEGHAFYHSFGRVLDGTACSPGAQGVCVAGRCLSAGCDGLLGSGALEDRCGRCGGANDSCLFVQRVFRDAGAFAGYWNVTLIPEGARHIRVEHRSRNHLALMGGDGRYVLNGHWVVSPPGTYEAAGTHVVYTRDTGPQETLQAAGPTSHDLLLQVLLQEPNPGIEFEFWLPRERYSPFQARVQALGWPLRQPQPRGVEPQPPAAPAVTPAQTPTLAPDPCPPCPDTRGRAHRLLHYCGSDFVFQARVLGHHHQAQETRYEVRIQLVYKNRSPLRAREYVWAPGHCPCPMLAPHRDYLMAVQRLVSPDGTQDQLLLPHAGYARPWSPAEDSRIRLTARRCPG |
| 预测分子量 | 56.0 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ADAMTSL5重组蛋白的虚构参考文献示例(仅供学术参考，非真实文献)：
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1. **文献名称**: *ADAMTSL5 Recombinant Protein Promotes Cardiomyocyte Extracellular Matrix Remodeling*
**作者**: Johnson, R. et al. (2018)
**摘要**: 本研究通过大肠杆菌表达系统成功制备了人源ADAMTSL5重组蛋白，并验证其在体外对心肌细胞外基质重塑的调控作用。实验表明，ADAMTSL5通过抑制TGF-β信号通路减少胶原沉积，提示其在心肌纤维化治疗中的潜在应用。
2. **文献名称**: *Structural and Functional Characterization of ADAMTSL5 in Skin Fibrosis*
**作者**: Lee, S. et al. (2019)
**摘要**: 利用哺乳动物细胞(HEK293)表达ADAMTSL5重组蛋白，解析其结构域对整合素结合的依赖性。体内实验表明，ADAMTSL5缺失加剧皮肤纤维化，而外源性重组蛋白可缓解模型小鼠的胶原过度积累。
3. **文献名称**: *ADAMTSL5 as a Novel Biomarker in Pulmonary Hypertension*
**作者**: Zhang, Y. et al. (2021)
**摘要**: 研究构建了ADAMTSL5重组蛋白的真核表达体系，发现其在肺动脉高压患者血清中显著下调。体外实验显示，重组ADAMTSL5通过调节血管平滑肌细胞的迁移能力，抑制病理性的血管重塑。
4. **文献名称**: *ADAMTSL5 Recombinant Protein Attenuates Hepatic Stellate Cell Activation*
**作者**: Smith, J. et al. (2020)
**摘要**: 通过昆虫细胞(Sf9)表达并纯化ADAMTSL5重组蛋白，证实其可结合肝星状细胞表面的LTBP1蛋白，抑制Wnt/β-catenin通路活性，从而减少肝脏纤维化标志物α-SMA的表达。
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注：以上文献为示例性内容，实际研究中请以真实发表的论文为准。
ADAMTSL5 (A Disintegrin and Metalloproteinase with Thrombospondin Motifs-like 5) is a secreted glycoprotein belonging to the ADAMTS/ADAMTSL superfamily, which regulates extracellular matrix (ECM) homeostasis and cellular signaling. Unlike canonical ADAMTS proteases, ADAMTSL5 lacks catalytic metalloproteinase domains but retains thrombospondin type-1 repeats (TSRs) critical for protein-protein interactions. It is encoded by the *ADAMTSL5* gene, located on human chromosome 19. and is expressed in tissues such as skin, heart, and skeletal muscle.
Functionally, ADAMTSL5 is implicated in ECM assembly, particularly through interactions with fibrillin microfibrils and proteoglycans. Studies suggest its role in modulating TGF-β signaling pathways, influencing cell adhesion, migration, and tissue remodeling. Mutations or dysregulation of ADAMTSL5 have been linked to genetic disorders like geleophysic dysplasia, a condition characterized by short stature, skeletal abnormalities, and cardiac defects, highlighting its importance in connective tissue integrity.
Recombinant ADAMTSL5 protein is engineered using mammalian expression systems (e.g., HEK293 or CHO cells) to ensure proper post-translational modifications, including glycosylation. The purified protein is utilized in biochemical assays, structural studies, and functional research to elucidate its interactions with ECM components or receptors. Its recombinant form also serves as a potential therapeutic agent or diagnostic biomarker in fibrosis-related diseases, cancer (where ECM remodeling is pathological), or connective tissue disorders.
Current research focuses on clarifying ADAMTSL5’s precise mechanisms, its interplay with other ECM proteins, and its therapeutic potential. As an understudied member of the ADAMTS/ADAMTSL family, it represents a promising target for understanding ECM-associated pathologies and developing targeted interventions.
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