纯度 | >95%SDS-PAGE. |
种属 | Human |
靶点 | PFKM |
Uniprot No | P08237 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 2-780aa |
氨基酸序列 | THEEHHAAKTLGIGKAIAVLTSGGDAQGMNAAVRAVVRVGIFTGARVFFV HEGYQGLVDGGDHIKEATWESVSMMLQLGGTVIGSARCKDFREREGRLRA AYNLVKRGITNLCVIGGDGSLTGADTFRSEWSDLLSDLQKAGKITDEEAT KSSYLNIVGLVGSIDNDFCGTDMTIGTDSALHRIMEIVDAITTTAQSHQR TFVLEVMGRHCGYLALVTSLSCGADWVFIPECPPDDDWEEHLCRRLSETR TRGSRLNIIIVAEGAIDKNGKPITSEDIKNLVVKRLGYDTRVTVLGHVQR GGTPSAFDRILGSRMGVEAVMALLEGTPDTPACVVSLSGNQAVRLPLMEC VQVTKDVTKAMDEKKFDEALKLRGRSFMNNWEVYKLLAHVRPPVSKSGSH TVAVMNVGAPAAGMNAAVRSTVRIGLIQGNRVLVVHDGFEGLAKGQIEEA GWSYVGGWTGQGGSKLGTKRTLPKKSFEQISANITKFNIQGLVIIGGFEA YTGGLELMEGRKQFDELCIPFVVIPATVSNNVPGSDFSVGADTALNTICT TCDRIKQSAAGTKRRVFIIETMGGYCGYLATMAGLAAGADAAYIFEEPFT IRDLQANVEHLVQKMKTTVKRGLVLRNEKCNENYTTDFIFNLYSEEGKGI FDSRKNVLGHMQQGGSPTPFDRNFATKMGAKAMNWMSGKIKESYRNGRIF ANTPDSGCVLGMRKRALVFQPVAELKDQTDFEHRIPKEQWWLKLRPILKI LAKYEIDLDTSDHAHLEHITRKRSGEAAVVDHHHHHH |
预测分子量 | 86 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PFKM重组蛋白的3篇模拟参考文献(非真实文献,仅供示例):
1. **《重组PFKM蛋白在大肠杆菌中的高效表达与纯化》**
作者:Zhang L. et al.
摘要:研究通过基因工程手段在大肠杆菌中表达人源PFKM重组蛋白,优化表达条件并利用亲和层析技术纯化,获得高纯度蛋白用于后续酶动力学分析。
2. **《PFKM结构解析及其变构调节机制研究》**
作者:Wang Y. & Chen H.
摘要:采用X射线晶体学解析重组PFKM蛋白的三维结构,揭示ATP和果糖-6磷酸结合位点,阐明其变构调节与糖酵解速率的关系。
3. **《PFKM缺失通过调控Warburg效应抑制肿瘤生长》**
作者:Kimura T. et al.
摘要:通过重组PFKM蛋白功能实验发现,PFKM敲低导致癌细胞糖酵解能力下降,乳酸生成减少,证实其在肿瘤代谢重编程中的关键作用。
**Background of PFKM Recombinant Protein**
Phosphofructokinase-1 (PFK-1), muscle type (PFKM), is a critical regulatory enzyme in glycolysis, catalyzing the irreversible conversion of fructose-6-phosphate to fructose-1.6-bisphosphate. This step is a major rate-limiting point in glycolysis, linking carbohydrate metabolism to cellular energy demands. PFKM is one of three isoforms (PFKM, PFKL, PFKP) that form tissue-specific tetrameric complexes, with PFKM predominating in skeletal muscle. Its activity is tightly regulated by allosteric effectors (e.g., ATP inhibition; AMP, ADP, and fructose-2.6-bisphosphate activation) and hormonal signals, ensuring metabolic flexibility under varying physiological conditions.
Genetic mutations in *PFKM* are linked to glycogen storage disease type VII (GSD VII/Tarui disease), a rare autosomal recessive disorder characterized by exercise intolerance, muscle cramps, and hemolytic anemia due to impaired glycolysis. Recombinant PFKM protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), enables detailed study of PFKM structure-function relationships, enzymatic kinetics, and mutation-driven pathologies. It is instrumental in screening potential therapeutics, such as enzyme stabilizers or activators, to address PFKM deficiencies.
The recombinant protein typically retains native enzymatic activity when properly folded and post-translationally modified (e.g., phosphorylation). Its production often involves affinity tags (e.g., His-tag) for purification, followed by functional validation. Beyond disease research, PFKM recombinant protein is used to investigate metabolic reprogramming in cancer, where upregulated glycolysis supports tumor growth. Additionally, it serves as a tool to explore PFKM’s role in insulin signaling, mitochondrial dysfunction, and metabolic disorders like diabetes.
Overall, PFKM recombinant protein is a vital resource for advancing understanding of glycolysis regulation, metabolic diseases, and therapeutic development.
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