| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | FN3KRP |
| Uniprot No | Q9HA64 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-309aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSMEELLRRELGCSSVRATGHSGGGCISQ GRSYDTDQGRVFVKVNPKAEARRMFEGEMASLTAILKTNTVKVPKPIKVL DAPGGGSVLVMEHMDMRHLSSHAAKLGAQLADLHLDNKKLGEMRLKEAGT VGRGGGQEERPFVARFGFDVVTCCGYLPQVNDWQEDWVVFYARQRIQPQM DMVEKESGDREALQLWSALQLKIPDLFRDLEIIPALLHGDLWGGNVAEDS SGPVIFDPASFYGHSEYELAIAGMFGGFSSSFYSAYHGKIPKAPGFEKRL QLYQLFHYLNHWNHFGSGYRGSSLNIMRNLVK |
| 预测分子量 | 37 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FN3KRP重组蛋白的假设性参考文献示例(注：文献为模拟生成，非真实存在)：
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1. **标题**: *Recombinant Expression and Enzymatic Characterization of Human FN3KRP*
**作者**: Smith A, et al.
**摘要**: 本研究成功在大肠杆菌中表达了具有活性的重组人FN3KRP蛋白，并通过质谱和酶动力学实验证实其能够催化果糖胺的磷酸化，揭示了其在非酶促糖基化产物代谢中的潜在作用。
2. **标题**: *Structural Insights into FN3KRP Substrate Specificity by X-ray Crystallography*
**作者**: Zhang L, et al.
**摘要**: 通过X射线晶体学解析了FN3KRP重组蛋白的三维结构，发现其活性口袋对果糖赖氨酸具有高度选择性，为设计调控该酶活性的化合物提供了结构基础。
3. **标题**: *FN3KRP Knockdown Exacerbates Diabetic Nephropathy in Mouse Models*
**作者**: Tanaka K, et al.
**摘要**: 利用重组FN3KRP蛋白进行体外补充实验，证明其可减少糖尿病小鼠肾脏中的晚期糖基化终产物(AGEs)积累，提示其在糖尿病并发症治疗中的潜在应用价值。
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**说明**：以上文献为示例性质，实际研究中建议通过PubMed、Web of Science等数据库检索真实发表的论文。若需具体文献协助，请提供更多研究背景。
Fructosamine 3-kinase-related protein (FN3KRP), also known as FN3K2 or AGK2. is a member of the fructosamine 3-kinase (FN3K) enzyme family. It shares structural homology with FN3K, which plays a role in mitigating non-enzymatic glycation of proteins by phosphorylating fructosamines—a process linked to diabetic complications. While FN3K primarily targets intracellular glycated proteins, FN3KRP exhibits distinct substrate preferences and enzymatic activity. Unlike FN3K, FN3KRP demonstrates broader substrate specificity, acting on ribulosamines and other ketoamine derivatives, suggesting a complementary role in cellular detoxification pathways.
FN3KRP is ubiquitously expressed, with higher levels in tissues such as the liver, kidney, and brain. Its recombinant form is typically produced using bacterial or mammalian expression systems, enabling studies on its biochemical properties and interactions. Recombinant FN3KRP retains enzymatic activity, facilitating investigations into its physiological relevance, particularly in conditions associated with oxidative stress and advanced glycation end-product (AGE) accumulation, such as diabetes, neurodegenerative disorders, and aging.
Research highlights FN3KRP’s potential regulatory role in metabolic homeostasis and cellular stress responses. However, its exact biological functions remain less characterized compared to FN3K. Studies using recombinant FN3KRP have explored its kinetic parameters, inhibitor sensitivity, and structural features, providing insights into substrate binding and catalytic mechanisms. These efforts aim to clarify its contribution to glycation repair pathways and therapeutic potential in metabolic diseases. Ongoing work seeks to unravel its interplay with FN3K and other detoxification systems, emphasizing its emerging significance in redox biology and disease pathogenesis.
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