| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PCSK9 |
| Uniprot No | Q8NBP7 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 31-692aa |
| 氨基酸序列 | QEDEDGDYEELVLALRSEEDGLAEAPEHGTTATFHRCAKDPWRLPGTYVV VLKEETHLSQSERTARRLQAQAARRGYLTKILHVFHGLLPGFLVKMSGDL LELALKLPHVDYIEEDSSVFAQSIPWNLERITPPRYRADEYQPPDGGSLV EVYLLDTSIQSDHREIEGRVMVTDFENVPEEDGTRFHRQASKCDSHGTHL AGVVSGRDAGVAKGASMRSLRVLNCQGKGTVSGTLIGLEFIRKSQLVQPV GPLVVLLPLAGGYSRVLNAACQRLARAGVVLVTAAGNFRDDACLYSPASA PEVITVGATNAQDQPVTLGTLGTNFGRCVDLFAPGEDIIGASSYCSTCFV SQSGTSQAAAHVAGIAAMMLSAEPELTLAELRQRLIHFSAKDVINEAWFP EDQRVLTPNLVAALPPSTHGAGWQLFCRTVWSAHSGPTRMATAVARCAPD EELLSCSSFSRSGKRRGERMEAQGGKLVCRAHNAFGGEGVYAIARCCLLP QANCSVHTAPPAEASMGTRVHCHQQGHVLTGCSSHWEVEDLGTHKPPVLR PRGQPNQCVGHREASIHASCCHAPGLECKVKEHGIPAPQEQVTVACEEGW TLTGCSALPGTSHVLGAYAVDNTCVVRSRDVSTTGSTSEGAVTAVAICCR SRHLAQASQELQ |
| 预测分子量 | 72 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3篇关于PCSK9重组蛋白的参考文献概览：
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1. **文献名称**：*"Structural and biochemical characterization of the wild-type PCSK9 protein and its natural mutants"*
**作者**：Cunningham D, et al.
**摘要**：该研究通过重组表达人源PCSK9蛋白，解析其晶体结构，揭示其与低密度脂蛋白受体(LDLR)结合的分子机制，并分析自然突变对功能的影响，为药物设计提供结构基础。
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2. **文献名称**：*"Antibody-based PCSK9 inhibition for cholesterol management: Insights from recombinant protein engineering"*
**作者**：Sabatine MS, et al.
**摘要**：通过重组DNA技术开发靶向PCSK9的单克隆抗体(如evolocumab)，临床试验表明其显著降低低密度脂蛋白胆固醇(LDL-C)水平，证实重组蛋白在心血管疾病治疗中的潜力。
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3. **文献名称**：*"Recombinant PCSK9 as a tool for studying LDL metabolism in vitro and in vivo"*
**作者**：Lagace TA, et al.
**摘要**：利用重组PCSK9蛋白建立细胞和小鼠模型，阐明PCSK9通过促进LDLR降解调控胆固醇稳态的机制，为代谢性疾病研究提供实验工具。
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**备注**：以上文献为代表性研究方向示例，实际引用需根据具体研究领域补充完整信息(期刊、年份等)。如需更详细文献，建议检索PubMed或Web of Science数据库。
**Background of PCSK9 Recombinant Protein**
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a serine protease primarily synthesized in the liver and involved in cholesterol metabolism. Discovered in 2003. PCSK9 gained prominence due to its role in regulating low-density lipoprotein receptor (LDLR) levels. It binds to LDLR on hepatocytes, promoting its lysosomal degradation, thereby reducing LDLR availability and increasing circulating LDL cholesterol (LDL-C). Elevated LDL-C is a key risk factor for cardiovascular diseases (CVD), making PCSK9 a therapeutic target.
Genetic studies revealed that gain-of-function PCSK9 mutations cause autosomal dominant hypercholesterolemia, while loss-of-function mutations correlate with reduced LDL-C and CVD risk. This dichotomy spurred drug development. Monoclonal antibodies (e.g., alirocumab, evolocumab) inhibiting PCSK9-LDLR interaction were approved, demonstrating significant LDL-C reduction. However, high costs and injection-based administration limited accessibility, driving interest in alternative strategies like small-molecule inhibitors, gene silencing, or recombinant protein-based approaches.
Recombinant PCSK9 proteins are engineered for research and therapeutic use. Produced via expression systems (e.g., mammalian cells), they retain biological activity and structural features of native PCSK9. These proteins serve as tools to study PCSK9-LDLR binding mechanisms, screen inhibitors, or develop vaccines. For instance, PCSK9-based vaccines aim to induce neutralizing antibodies, mimicking natural loss-of-function mutations.
Despite progress, challenges remain in optimizing stability, delivery, and cost-effectiveness. Ongoing research explores fusion proteins, peptide mimetics, and CRISPR-based editing to enhance therapeutic potential. PCSK9 recombinant proteins continue to bridge translational gaps, offering insights into lipid metabolism and paving the way for next-generation CVD therapies.
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