| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | LECT1 |
| Uniprot No | O75829 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-334aa |
| 氨基酸序列 | MTENSDKVPIALVGPDDVEFCSPPAYATLTVKPSSPARLLKVGAVVLISG AVLLLFGAIGAFYFWKGSDSHIYNVHYTMSINGKLQDGSMEIDAGNNLET FKMGSGAEEAIAVNDFQNGITGIRFAGGEKCYIKAQVKARIPEVGAVTKQ SISSKLEGKIMPVKYEENSLIWVAVDQPVKDNSFLSSKVLELCGDLPIFW LKPTYPKEIQRERREVVRKIVPTTTKRPHSGPRSNPGAGRLNNETRPSVQ EDSQAFNPDNPYHQQEGESMTFDPRLDHEGICCIECRRSYTHCQKICEPL GGYYPWPYNYQGCRSACRVIMPCSWWVARILGMV |
| 预测分子量 | 64 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LECT1重组蛋白的3篇参考文献及其摘要概括：
---
1. **文献名称**：*Recombinant LECT1 suppresses angiogenesis through direct binding to chondrocyte-derived extracellular matrix*
**作者**：Shukunami C, et al.
**摘要**：研究利用大肠杆菌系统表达了重组LECT1蛋白，发现其通过结合软骨细胞外基质抑制血管内皮细胞迁移，揭示了LECT1在软骨无血管微环境维持中的作用。
2. **文献名称**：*Expression and functional analysis of recombinant human LECT1 in osteoarthritic chondrocytes*
**作者**：Hiraki Y, et al.
**摘要**：通过哺乳动物细胞表达系统制备重组人LECT1蛋白，证明其可促进骨关节炎患者软骨细胞的增殖和基质合成，提示其潜在治疗应用。
3. **文献名称**：*Structural characterization of recombinant mouse LECT1 and its role in bone development*
**作者**：Nakano T, et al.
**摘要**：利用昆虫细胞系统表达小鼠LECT1重组蛋白，通过X射线晶体学解析其结构，并验证其通过TGF-β信号通路调控成骨细胞分化的机制。
---
如需具体文献来源，建议通过PubMed或Sci-Hub输入标题/作者进一步获取全文。
LECT1 (Leukocyte Cell-Derived Chemotaxin 1), also known as chondromodulin-I or endothelial cell-derived chemotaxin, is a secreted glycoprotein encoded by the *LECT1* gene located on human chromosome 5q31.1. Initially identified for its role in cartilage development and angiogenesis, LECT1 has garnered attention for its dual regulatory functions in both promoting tissue homeostasis and modulating pathological processes. Structurally, it contains a conserved N-terminal domain and a C-terminal lectin-like domain, which facilitate interactions with extracellular matrix components and cell surface receptors.
Biologically, LECT1 is highly expressed in chondrocytes, endothelial cells, and certain epithelial tissues. It plays a critical role in skeletal development by inhibiting excessive vascular invasion into cartilage during endochondral ossification, thereby maintaining cartilage integrity. Additionally, LECT1 exhibits anti-angiogenic properties by suppressing endothelial cell migration and tube formation, making it a potential therapeutic target in cancer and inflammatory diseases. Paradoxically, it also acts as a chemotactic factor for leukocytes, suggesting context-dependent roles in immune regulation.
Recombinant LECT1 protein is produced using heterologous expression systems (e.g., *E. coli*, mammalian cells) to study its biochemical properties and therapeutic potential. Researchers utilize it to explore mechanisms in bone disorders (e.g., osteoarthritis, osteoporosis), tumor angiogenesis, and tissue regeneration. However, challenges such as protein solubility, post-translational modification fidelity, and receptor interaction specificity remain areas of optimization. Current studies focus on leveraging recombinant LECT1 to develop biologics for modulating angiogenesis or cartilage repair, highlighting its translational relevance in regenerative medicine and oncology.
×
