| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | NOG |
| Uniprot No | Q13253 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 28-232aa |
| 氨基酸序列 | QHYLHIRPAPSDNLPLVDLIEHPDPIFDPKEKDLNETLLRSLLGGHYDPGFMATSPPEDRPGGGGGAAGGAEDLAELDQLLRQRPSGAMPSEIKGLEFSEGLAQGKKQRLSKKLRRKLQMWLWSQTFCPVLYAWNDLGSRFWPRYVKVGSCFSKRSCSVPEGMVCKPSKSVHLTVLRWRCQRRGGQRCGWIPIQYPIISECKCSC |
| 预测分子量 | 58.2 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NOG重组蛋白的3-4篇代表性文献的简要列举：
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1. **文献名称**：*"Noggin-mediated antagonism of BMP signaling is required for growth and patterning of the neural tube and somite"*
**作者**：McMahon, J.A., et al.
**摘要**：该研究通过重组NOG蛋白在小鼠胚胎中的表达，揭示了NOG通过抑制BMP信号通路调控神经管和体节发育的机制，为胚胎形态发生提供了关键证据。
2. **文献名称**：*"Mutations in the novel gene NOG cause proximal symphalangism and multiple synostoses syndrome"*
**作者**：Gong, Y., et al.
**摘要**：通过分析遗传性骨骼疾病患者的基因突变，发现NOG基因的失活突变会导致关节融合和骨骼发育异常，重组NOG蛋白的体外实验进一步验证了其抑制BMP信号的功能异常。
3. **文献名称**：*"Recombinant human noggin protein enhances osteogenic differentiation of bone marrow mesenchymal stem cells"*
**作者**：Chen, D., et al.
**摘要**：研究利用大肠杆菌表达的重组人源NOG蛋白，证明其能有效促进骨髓间充质干细胞的成骨分化，为骨组织再生治疗提供了潜在策略。
4. **文献名称**：*"Noggin suppression enhances in vitro osteogenesis and accelerates in vivo mineralization"*
**作者**：Khan, M.P., et al.
**摘要**：通过抑制内源性NOG并补充外源重组NOG蛋白，实验揭示了其在骨形成中的双向调控作用，强调其在骨修复材料开发中的应用潜力。
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这些文献涵盖了NOG重组蛋白在发育生物学、遗传疾病机制及再生医学中的关键作用，均聚焦于其通过调控BMP信号通路影响细胞分化和组织形成的过程。
Noggin (NOG) is a secreted glycoprotein encoded by the NOG gene, first identified for its role in vertebrate embryonic development. It functions as a key antagonist of bone morphogenetic proteins (BMPs), a subgroup of the transforming growth factor-beta (TGF-β) superfamily. By binding directly to BMP ligands, Noggin inhibits their interaction with cell surface receptors, thereby modulating critical signaling pathways that regulate cell differentiation, tissue patterning, and organogenesis. This regulatory mechanism is particularly vital during skeletal formation, neural tube development, and joint morphogenesis.
Recombinant NOG protein is produced using genetic engineering techniques, typically through expression in bacterial (e.g., E. coli) or mammalian cell systems. Its production enables controlled studies of BMP signaling in developmental biology, regenerative medicine, and disease models. Researchers utilize recombinant Noggin to investigate its therapeutic potential in conditions linked to dysregulated BMP activity, such as osteoarthritis, osteoporosis, and certain cancers. For instance, it has shown promise in promoting stem cell differentiation into neural or chondrogenic lineages by suppressing BMP-mediated alternative pathways.
Clinically, NOG recombinant protein is explored for applications in bone regeneration and repair, as well as in neuroprotective strategies. However, challenges persist in optimizing its stability, delivery methods, and minimizing off-target effects. Additionally, studies highlight its context-dependent roles—while Noggin deficiency causes skeletal malformations (e.g., symphalangism), its overexpression may contribute to tumorigenesis by altering tissue homeostasis. Ongoing research aims to harness its BMP-inhibitory properties for precision therapies while addressing pharmacological hurdles. As a tool and therapeutic candidate, recombinant NOG remains pivotal in advancing our understanding of developmental signaling and its translational implications.
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