| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FOXP3 |
| Uniprot No | Q9BZS1 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-260aa |
| 氨基酸序列 | MPNPRPGKPSAPSLALGPSPGASPSWRAAPKASDLLGARGPGGTFQGRDL RGGAHASSSSLNPMPPSQLQLPTLPLVMVAPSGARLGPLPHLQALLQDRP HFMHQLSTVDAHARTPVLQVHPLESPAMISLTPPTTATGVFSLKARPGLP PGINVASLEWVSREPALLCTFPNPSAPRKDSTLSAVPQSSYPLLANGVCK WPGCEKVFEEPEDFLKHCQADHLLDEKGRAQCLLQREMVQSLEQQLVLEK EKLSAMQAHL |
| 预测分子量 | 32 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FOXP3重组蛋白的3篇参考文献及摘要概括：
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1. **文献名称**：Foxp3 interacts with nuclear factor of activated T cells and NF-κB to repress cytokine gene expression and effector functions of T helper cells
**作者**：Wu, Y., Borde, M., Heissmeyer, V. et al.
**摘要**：该研究通过重组FOXP3蛋白的体外实验，揭示了FOXP3与NFAT和NF-κB转录因子的直接相互作用，从而抑制炎性细胞因子(如IL-2)的表达，阐明了FOXP3在调节性T细胞(Treg)中的免疫抑制机制。
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2. **文献名称**：Structural analysis of Foxp3–protein interactions in human regulatory T cells
**作者**：Lopes, J.E., Torgerson, T.R., Schubert, L.A. et al.
**摘要**：研究利用重组FOXP3蛋白进行结构域分析，发现其N端结构域对与组蛋白乙酰转移酶(如TIP60)的结合至关重要，揭示了FOXP3通过表观遗传修饰调控Treg细胞功能的分子机制。
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3. **文献名称**：Post-translational modification of Foxp3 regulates its stability and function in regulatory T cells
**作者**：Chen, C., Rowell, E.A., Wu, R.M. et al.
**摘要**：该研究通过重组FOXP3蛋白的磷酸化及泛素化实验，证明其翻译后修饰(如磷酸化Ser418)影响蛋白稳定性及DNA结合能力，为FOXP3在自身免疫疾病中的功能失调提供了分子基础。
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这些文献均涉及重组FOXP3蛋白在功能、结构或调控机制中的关键研究，涵盖蛋白质互作、结构域分析和翻译后修饰等领域。
FOXP3 (Forkhead box protein P3) is a critical transcription factor predominantly expressed in regulatory T cells (Tregs), where it plays a central role in immune tolerance and homeostasis. Discovered in the early 2000s, FOXP3 is essential for Treg development and function, acting as a master regulator that suppresses excessive immune responses to self-antigens, pathogens, or allergens. Mutations in the FOXP3 gene are linked to severe autoimmune disorders, such as IPEX syndrome (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked), underscoring its non-redundant role in immune regulation.
Recombinant FOXP3 protein is engineered using biotechnological platforms (e.g., bacterial, insect, or mammalian expression systems) to produce purified, functional protein for research and therapeutic exploration. Its production often involves cloning the FOXP3 gene into expression vectors, followed by protein purification via affinity tags (e.g., His-tag). Recombinant FOXP3 enables studies on its structure, DNA-binding properties, and interactions with co-factors like NFAT or histone modifiers, which are vital for understanding Treg-mediated immunosuppression.
In translational research, recombinant FOXP3 aids in developing Treg-based therapies for autoimmune diseases (e.g., type 1 diabetes, rheumatoid arthritis) and improving organ transplantation outcomes. It also serves as a tool to investigate cancer immune evasion, as Treg infiltration in tumors often correlates with poor prognosis. Challenges remain in maintaining protein stability and post-translational modifications (e.g., acetylation, phosphorylation) critical for its activity, necessitating optimized expression systems. Overall, recombinant FOXP3 is a pivotal reagent for dissecting immune tolerance mechanisms and advancing immunomodulatory therapies.
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