首页 / 产品 / 蛋白 / 细胞因子、趋化因子与生长因子
| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RANkL |
| Uniprot No | O14788 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 152-317aa |
| 氨基酸序列 | LDLAKRSKLEAQPFAHLTINATDIPSGSHKVSLSSWYHDRGWAKISNMTF SNGKLIVNQDGFYYLYANICFRHHETSGDLATEYLQLMVYVTKTSIKIPS SHTLMKGGSTKYWSGNSEFHFYSINVGGFFKLRSGEEISIEVSNPSLLDP DQDATYFGAFKVRDID |
| 预测分子量 | 18 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RANKL重组蛋白的3篇参考文献的简要概括：
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1. **文献名称**: *Osteoprotegerin Ligand Is a Cytokine That Regulates Osteoclast Differentiation and Activation*
**作者**: Lacey, D.L., et al.
**摘要**: 该研究首次阐明RANKL(重组蛋白形式)通过结合RANK受体调控破骨细胞分化和骨吸收功能，为骨质疏松症治疗靶点奠定基础。实验证明重组RANKL可直接诱导小鼠骨髓细胞分化为破骨细胞。
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2. **文献名称**: *Activated T Cells Regulate Bone Loss and Joint Destruction in Adjuvant Arthritis through Osteoprotegerin Ligand*
**作者**: Kong, Y.Y., et al.
**摘要**: 研究利用重组RANKL蛋白验证其在炎症性关节炎中的作用，发现T细胞通过分泌RANKL介导关节周围骨破坏，阻断RANKL可显著减少动物模型中的骨质流失。
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3. **文献名称**: *Recombinant human RANKL expands CD34+ hematopoietic progenitor cells and enhances osteoclastogenesis in vitro*
**作者**: Sutherland, H., et al.
**摘要**: 该文献描述重组人RANKL蛋白在体外扩增造血干细胞并促进破骨细胞生成的应用，为研究骨代谢疾病及药物筛选提供了可靠实验体系。
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*注：以上文献均发表于1997-2002年间，是RANKL功能研究的奠基性工作，涉及《Cell》《Nature》等期刊。如需具体发表年份或补充文献，可进一步提供。*
**Background of RANKL Recombinant Protein**
Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL), also known as TNF-related activation-induced cytokine (TRANCE) or osteoclast differentiation factor (ODF), is a transmembrane protein belonging to the tumor necrosis factor (TNF) superfamily. It plays a pivotal role in regulating bone remodeling, immune cell differentiation, and lymph node development. RANKL exists as a homotrimeric protein that binds to its receptor RANK (Receptor Activator of Nuclear Factor Kappa-Β) on osteoclast precursors, triggering signaling cascades essential for osteoclast formation, activation, and survival. This interaction is critical for bone resorption, and dysregulation of the RANKL-RANK axis is implicated in osteoporosis, rheumatoid arthritis, and cancer-induced bone metastasis.
Recombinant RANKL proteins are engineered using expression systems (e.g., mammalian, insect, or bacterial cells) to produce soluble, bioactive forms of the protein. These recombinant variants retain the functional trimeric structure and are widely utilized in research to study osteoclastogenesis, bone metabolism, and immune regulation. For therapeutic applications, RANKL inhibition (e.g., using monoclonal antibodies like denosumab) has become a clinical strategy to treat bone loss disorders. Conversely, recombinant RANKL itself is employed in vitro to induce osteoclast differentiation from precursor cells, enabling mechanistic studies or drug screening.
The development of recombinant RANKL has also advanced understanding of its interplay with osteoprotegerin (OPG), a decoy receptor that neutralizes RANKL to prevent excessive bone resorption. This balance between RANKL and OPG is a key focus in bone pathophysiology. Today, recombinant RANKL remains a vital tool in both basic research and translational medicine, bridging insights into skeletal biology, immunology, and oncology.
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