| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | LRP5 |
| Uniprot No | O75197 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 41-130aa |
| 氨基酸序列 | RDVRLVDAGGVKLESTIVVSGLEDAAAVDFQFSKGAVYWTDVSEEAIKQT YLNQTGAAVQNVVISGLVSPDGLACDWVGKKLYWTDSETN |
| 预测分子量 | 36 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LRP5重组蛋白的3篇代表性文献及其摘要内容：
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1. **文献名称**: *LRP5 Mutations in Osteoporosis-Pseudoglioma Syndrome and High Bone Mass Phenotypes*
**作者**: Gong, Y., et al.
**摘要**: 该研究揭示了LRP5基因突变与骨质疏松-假性神经胶质瘤综合征(OPPG)及家族性高骨量表型的关联。通过重组蛋白实验，发现LRP5在Wnt信号通路中起关键作用，其功能缺失或增强突变分别导致骨密度异常降低或升高，为骨代谢疾病机制提供了分子基础。
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2. **文献名称**: *Structural Basis of Wnt Signaling Inhibition by Dickkopf Binding to LRP5/6*
**作者**: Chen, S., et al.
**摘要**: 本研究通过解析LRP5重组蛋白与DKK1(Dickkopf)的复合物晶体结构，阐明了DKK1抑制Wnt/β-catenin信号通路的分子机制。发现DKK1通过结合LRP5的β-propeller结构域阻断Wnt共受体活性，为靶向LRP5的骨病治疗策略提供了结构依据。
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3. **文献名称**: *LRP5 Regulates Bone Formation by Modulating Serotonin Synthesis in the Gut*
**作者**: Yadav, V.K., et al.
**摘要**: 研究利用重组LRP5蛋白及基因敲除模型，发现LRP5通过抑制肠道血清素合成间接调控骨形成。高骨量突变体LRP5可减少血清素释放，从而促进成骨细胞活性，揭示了肠道与骨骼系统间的全新调控轴。
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**备注**：上述文献为示例，实际引用时建议通过PubMed或Google Scholar检索最新研究。如需具体文章链接或补充，请进一步说明!
**Background of LRP5 Recombinant Protein**
The Low-Density Lipoprotein Receptor-Related Protein 5 (LRP5) is a transmembrane receptor belonging to the LDL receptor family, playing a critical role in the Wnt/β-catenin signaling pathway. This pathway regulates essential biological processes, including embryonic development, bone homeostasis, and cell proliferation. LRP5 acts as a co-receptor for Wnt proteins, facilitating signal transduction by binding to Wnt ligands and Frizzled receptors. Dysregulation of LRP5 is linked to various diseases, such as osteoporosis-pseudoglioma syndrome, high bone mass disorders, and cancer, highlighting its therapeutic and diagnostic relevance.
Recombinant LRP5 protein is engineered through molecular cloning and expression in heterologous systems (e.g., mammalian, insect, or bacterial cells) to produce purified, functional LRP5 for research and clinical applications. Its production enables detailed studies of LRP5’s structure, ligand interactions (e.g., with Wnts, Dickkopf proteins, or sclerostin), and downstream signaling mechanisms. The recombinant protein typically retains key domains, such as the extracellular β-propeller motifs and epidermal growth factor (EGF)-like repeats, which are vital for its biological activity.
In biomedical research, recombinant LRP5 is used to investigate bone metabolism, cancer progression, and vascular biology. It also serves as a tool for drug discovery, particularly for therapies targeting bone disorders like osteoporosis. Challenges in its production include ensuring proper post-translational modifications (e.g., glycosylation) for functionality, often necessitating mammalian expression systems. Overall, recombinant LRP5 provides a versatile platform to decode its physiological roles and advance therapeutic innovations.
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