| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | QDPR |
| Uniprot No | P09417 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2-244aa |
| 氨基酸序列 | AAAAAAGEA RRVLVYGGRG ALGSRCVQAF RARNWWVASV DVVENEEASA SIIVKMTDSF TEQADQVTAE VGKLLGEEKV DAILCVAGGW AGGNAKSKSL FKNCDLMWKQ SIWTSTISSH LATKHLKEGG LLTLAGAKAA LDGTPGMIGY GMAKGAVHQL CQSLAGKNSG MPPGAAAIAV LPVTLDTPMN RKSMPEADFS SWTPLEFLVE TFHDWITGKN RPSSGSLIQV VTTEGRTELT PAYF |
| 预测分子量 | 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QDPR重组蛋白的3篇代表性文献摘要：
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1. **文献名称**：*Cloning and expression of human quinoid dihydropteridine reductase*
**作者**：Thöny, B., Leimbacher, W., Blau, N. et al.
**摘要**：该研究首次报道了人类QDPR基因的cDNA克隆，并在大肠杆菌中实现了重组表达。重组蛋白表现出与天然酶相似的催化活性，为后续研究QDPR缺陷型苯丙酮尿症提供了工具。
2. **文献名称**：*Functional characterization of recombinant human QDPR in a eukaryotic expression system*
**作者**：Li, J., Wang, Y., Zhang, H.
**摘要**：作者在HEK293细胞中表达了带有标签的重组QDPR蛋白，并验证了其在四氢生物蝶呤(BH4)再生中的功能。研究还发现特定突变会显著降低酶活性，解释了部分遗传性代谢疾病的分子机制。
3. **文献名称**：*Crystallographic analysis of QDPR reveals structural basis for enzymatic regulation*
**作者**：Müller, T., Schulze, A., Huber, R.
**摘要**：通过X射线晶体学解析了重组QDPR蛋白的三维结构，揭示了其底物结合域和潜在的调控位点，为开发小分子抑制剂或治疗策略提供了结构依据。
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注：以上文献为示例性质，实际引用时需核对具体来源及发表年份。如需最新研究，建议在PubMed或Web of Science中以“QDPR recombinant protein”为关键词检索。
**Background of QDPR Recombinant Protein**
QDPR (quinoid dihydropteridine reductase) is a critical enzyme in the metabolic pathway responsible for recycling tetrahydrobiopterin (BH4), an essential cofactor for aromatic amino acid hydroxylases, including phenylalanine hydroxylase (PAH), tyrosine hydroxylase, and tryptophan hydroxylase. BH4 is required for the synthesis of neurotransmitters like dopamine, serotonin, and norepinephrine, as well as the metabolism of phenylalanine. QDPR specifically catalyzes the NADH-dependent reduction of quinonoid dihydrobiopterin to BH4. ensuring its regeneration and availability for cellular processes.
Mutations in the *QDPR* gene lead to QDPR deficiency, a rare autosomal recessive disorder associated with hyperphenylalaninemia and neurotransmitter depletion. This condition, classified as a form of BH4-deficient phenylketonuria (PKU), manifests with neurological symptoms such as developmental delays, seizures, and movement disorders. Early diagnosis and intervention, including BH4 supplementation or dietary management, are critical to mitigate long-term complications.
Recombinant QDPR protein is produced using biotechnological methods, such as expression in *E. coli* or mammalian cell systems, to generate a purified, functional enzyme for research and therapeutic applications. It serves as a vital tool for studying BH4 metabolism, enzyme kinetics, and the molecular mechanisms underlying QDPR-related disorders. Additionally, recombinant QDPR holds potential in enzyme replacement therapy (ERT) strategies to address QDPR deficiency, offering a targeted approach to restore BH4 homeostasis.
Research on QDPR recombinant protein also contributes to drug discovery, particularly in designing small-molecule chaperones or stabilizers to enhance mutant QDPR activity. Its role in neurotransmitter synthesis further links it to broader studies on neurological and metabolic diseases, emphasizing its importance in both basic science and clinical innovation.
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