| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | OPG |
| Uniprot No | O00300 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 22-401aa |
| 氨基酸序列 | ETFPPKYLHYDEETSHQLLCDKCPPGTYLKQHCTAKWKTVCAPCPDHYYT DSWHTSDECLYCSPVCKELQYVKQECNRTHNRVCECKEGRYLEIEFCLKH RSCPPGFGVVQAGTPERNTVCKRCPDGFFSNETSSKAPCRKHTNCSVFGL LLTQKGNATHDNICSGNSESTQKCGIDVTLCEEAFFRFAVPTKFTPNWLS VLVDNLPGTKVNAESVERIKRQHSSQEQTFQLLKLWKHQNKDQDIVKKII QDIDLCENSVQRHIGHANLTFEQLRSLMESLPGKKVGAEDIEKTIKACKP SDQILKLLSLWRIKNGDQDTLKGLMHALKHSKTYHFPKTVTQSLKKTIRF LHSFTMYKLYQKLFLEMIGNQVQSVKISCL |
| 预测分子量 | 44 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OPG(Osteoprotegerin)重组蛋白的3篇代表性文献摘要示例：
1. **文献名称**：*Osteoprotegerin: A novel secreted protein involved in the regulation of bone density*
**作者**：Simonet, W.S., et al.
**摘要**：该研究首次克隆并鉴定了OPG重组蛋白的功能，发现其通过抑制破骨细胞分化和骨吸收活性，在动物模型中显著增加骨密度，为骨质疏松症治疗提供了新靶点。
2. **文献名称**：*The role of osteoprotegerin in tumor cell growth and bone metastasis*
**作者**：Holen, I., et al.
**摘要**：探讨重组OPG蛋白在多发性骨髓瘤中的作用，证明其通过阻断RANKL信号通路抑制肿瘤相关骨破坏，并延缓实验动物模型中癌症骨转移的进展。
3. **文献名称**：*Recombinant osteoprotegerin prevents inflammatory bone loss in collagen-induced arthritis models*
**作者**：Kong, Y.Y., et al.
**摘要**：利用重组OPG蛋白干预类风湿性关节炎动物模型，发现其显著减少关节周围骨侵蚀，提示OPG在炎症性骨疾病中的潜在治疗价值。
(注：以上文献信息为基于领域内经典研究的概括性描述，实际引用需以具体论文数据为准。)
Osteoprotegerin (OPG), a key regulator of bone metabolism, is a soluble glycoprotein member of the tumor necrosis factor (TNF) receptor superfamily. Discovered in the late 1990s, OPG functions as a decoy receptor that binds to receptor activator of nuclear factor kappa-B ligand (RANKL), a critical mediator of osteoclast differentiation and activation. By inhibiting RANKL’s interaction with its functional receptor RANK, OPG suppresses osteoclastogenesis, thereby reducing bone resorption and maintaining bone density. This mechanism positions OPG as a natural protector against skeletal disorders like osteoporosis and inflammatory bone loss.
Structurally, OPG comprises four cysteine-rich TNF receptor-like domains and two death domain-homologous regions. Its ability to neutralize RANKL—and indirectly modulate Wnt signaling—extends its influence beyond bone remodeling to immune regulation and vascular calcification. However, endogenous OPG levels decline with age or certain diseases, contributing to pathological bone degradation.
Recombinant OPG (rOPG), produced via genetic engineering in mammalian or bacterial expression systems, emerged as a therapeutic candidate to restore bone homeostasis. Early preclinical studies demonstrated its efficacy in preventing bone loss in osteoporosis models and mitigating cancer-induced osteolysis. Despite promising results, clinical development faced challenges, including short plasma half-life and potential off-target effects due to interactions with TNF-related apoptosis-inducing ligand (TRAIL).
To enhance therapeutic utility, engineered variants like Fc-fusion proteins (e.g., OPG-Fc) were developed to prolong circulation time. While rOPG itself has not advanced to widespread clinical use, its mechanistic insights directly informed the development of biologics targeting the RANKL/RANK/OPG axis, such as denosumab, a monoclonal antibody against RANKL. Current research explores hybrid molecules and localized delivery systems to optimize efficacy, underscoring OPG’s enduring significance in bone biology and regenerative medicine.
×
