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| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FGF23 |
| Uniprot No | Q9GZV9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 25-251aa |
| 氨基酸序列 | YPNASPLLGSSWGGLIHLYTATARNSYHLQIHKNGHVDGAPHQTIYSALM IRSEDAGFVVITGVMSRRYLCMDFRGNIFGSHYFDPENCRFQHQTLENGY DVYHSPQYHFLVSLGRAKRAFLPGMNPPPYSQFLSRRNEIPLIHFNTPIP RRHTRSAEDDSERDPLNVLKPRARMTPAPASCSQELPSAEDNSPMASDPL GVVRGGRVNTHAGGTGPEGCRPFAKFI |
| 预测分子量 | 25 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3-4条关于FGF23重组蛋白的参考文献及其摘要概括：
1. **"FGF23 is a potent regulator of vitamin D metabolism and phosphate homeostasis"**
- **作者**: Shimada T, et al.
- **摘要**: 该研究首次阐明重组FGF23蛋白通过抑制肾脏1α-羟化酶活性减少活性维生素D的合成，并抑制肾小管对磷酸盐的重吸收，揭示了其在调节磷代谢中的核心作用。
2. **"Recombinant FGF23 suppresses phosphate transport in renal epithelial cells"**
- **作者**: Yamazaki Y, et al.
- **摘要**: 研究利用重组FGF23蛋白，证明其通过下调肾脏钠-磷酸盐共转运蛋白(NaPi-IIa)的表达，直接调控磷酸盐排泄，为遗传性低磷血症的机制研究提供依据。
3. **"Role of FGF23 in chronic kidney disease: Pathophysiology and therapeutic implications"**
- **作者**: Gutiérrez OM, et al.
- **摘要**: 分析重组FGF23在慢性肾病(CKD)模型中的作用，发现其水平升高与心血管并发症相关，提示靶向FGF23可能成为改善CKD患者预后的策略。
4. **"Anti-FGF23 neutralizing antibodies ameliorate hypophosphatemic rickets in murine models"**
- **作者**: Aono Y, et al.
- **摘要**: 研究开发针对FGF23过量的重组抗体药物，证明其可恢复低磷血症模型小鼠的血磷水平，为X-连锁低磷性佝偻病(XLH)的临床治疗提供新方向。
以上文献涵盖FGF23重组蛋白的生理功能、疾病机制及治疗应用，均为基础与转化研究中的关键论文。
Fibroblast Growth Factor 23 (FGF23) is a hormone primarily secreted by osteocytes and osteoblasts, playing a critical role in phosphate and vitamin D homeostasis. It regulates renal phosphate excretion by binding to the α-Klotho-FGF receptor complex in the proximal tubules, suppressing phosphate reabsorption and 1.25-dihydroxyvitamin D synthesis. Dysregulation of FGF23 is linked to several disorders. Elevated FGF23 levels are associated with hypophosphatemic conditions, such as X-linked hypophosphatemia (XLH) and chronic kidney disease (CKD), where excessive phosphate wasting leads to bone mineralization defects. Conversely, FGF23 deficiency or resistance causes hyperphosphatemia, as seen in familial tumoral calcinosis.
Recombinant FGF23 protein, produced via mammalian expression systems (e.g., CHO or HEK293 cells), is engineered to mimic the native protein’s biological activity. It serves as a vital tool for studying FGF23 signaling pathways, drug screening, and developing therapeutic interventions. For instance, anti-FGF23 antibodies (e.g., burosumab) are used to treat XLH by neutralizing excess FGF23 activity. Conversely, recombinant FGF23 could theoretically address conditions caused by its deficiency, though clinical applications remain exploratory.
In diagnostics, recombinant FGF23 aids in standardizing assays to measure circulating FGF23 levels, critical for differentiating renal phosphate disorders. Challenges persist in therapeutic use due to FGF23’s short half-life and pleiotropic effects, prompting research into engineered variants with improved stability and tissue specificity. Additionally, understanding its interactions with co-receptors and downstream effectors may unveil targeted therapies for mineral metabolism disorders. Overall, recombinant FGF23 bridges basic research and clinical innovation, offering insights into phosphate-related pathologies and potential treatment avenues.
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