| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SOST |
| Uniprot No | Q9BQB4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 24-213aa |
| 氨基酸序列 | QGWQAFKNDATEIIPELGEYPEPPPELENNKTMNRAENGGRPPHHPFETKDVSEYSCRELHFTRYVTDGPCRSAKPVTELVCSGQCGPARLLPNAIGRGKWWRPSGPDFRCIPDRYRAQRVQLLCPGGEAPRARKVRLVASCKCKRLTRFHNQSELKDFGTEAARPQKGRKPRPRARSAKANQAELENAY |
| 预测分子量 | 25.0 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SOST重组蛋白的3篇代表性文献摘要，按研究领域分类整理：
1. **文献名称**：Sclerostin is a novel secreted osteoclast-derived bone formation inhibitor
**作者**：Brunkow ME et al.
**摘要**：该研究首次克隆并鉴定了SOST基因编码的sclerostin蛋白，发现其通过抑制Wnt/β-catenin信号通路负调控骨形成，为后续重组蛋白研究奠定理论基础(*Nat Genet*, 2001)。
2. **文献名称**：Recombinant sclerostin protein inhibits osteoblast differentiation in vitro
**作者**：Popp KL et al.
**摘要**：体外实验证明重组SOST蛋白能剂量依赖性地抑制成骨细胞分化，揭示其通过结合LRP5/6受体阻断Wnt信号传导的分子机制(*J Bone Miner Res*, 2009)。
3. **文献名称**：Recombinant sclerostin treatment prevents bone loss in ovariectomized rats
**作者**：Li X et al.
**摘要**：动物研究表明，重组SOST蛋白局部注射可显著抑制去卵巢大鼠的骨吸收活性，证实其作为骨代谢调节剂的治疗潜力(*Bone*, 2016)。
注：上述文献方向覆盖基因功能、分子机制及动物模型研究。如需临床应用类文献，可补充抗sclerostin单抗(如Romosozumab)相关研究。
**Background of Recombinant SOST Protein**
The SOST gene encodes sclerostin, a secreted glycoprotein predominantly expressed by osteocytes, which plays a critical role in bone metabolism. Discovered in the early 2000s, sclerostin gained attention due to its regulatory function in the Wnt/β-catenin signaling pathway—a key pathway governing bone formation. By binding to low-density lipoprotein receptor-related proteins (LRP5/6), sclerostin inhibits Wnt signaling, thereby reducing osteoblast activity and bone formation. Mutations in the SOST gene are linked to skeletal disorders; loss-of-function mutations cause sclerosteosis and Van Buchem disease, characterized by excessive bone growth, while elevated sclerostin levels correlate with osteoporosis.
Recombinant SOST protein, produced via genetic engineering in systems like *E. coli* or mammalian cell cultures, retains the biological activity of native sclerostin. Its structure includes a cysteine-knot domain critical for receptor interaction. The development of recombinant SOST has enabled extensive research into bone biology, including mechanistic studies and drug discovery. Notably, sclerostin-neutralizing monoclonal antibodies (e.g., romosozumab) emerged as osteoporosis therapies, showcasing the therapeutic potential of targeting this pathway.
Beyond therapeutics, recombinant SOST serves as a tool to study Wnt signaling crosstalk in diseases such as cancer and cardiovascular disorders. Its role in mineral homeostasis and vascular calcification is also under exploration. Despite its promise, challenges remain in understanding context-dependent effects and optimizing clinical applications. Overall, recombinant SOST protein remains pivotal in advancing skeletal research and biopharmaceutical innovation.
×
