纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | F12 |
Uniprot No | P00748 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 20-372aa |
氨基酸序列 | IPPWEAPKEHKYKAEEHTVVLTVTGEPCHFPFQYHRQLYHKCTHKGRPGPQPWCATTPNFDQDQRWGYCLEPKKVKDHCSKHSPCQKGGTCVNMPSGPHCLCPQHLTGNHCQKEKCFEPQLLRFFHKNEIWYRTEQAAVARCQCKGPDAHCQRLASQACRTNPCLHGGRCLEVEGHRLCHCPVGYTGAFCDVDTKASCYDGRGLSYRGLARTTLSGAPCQPWASEATYRNVTAEQARNWGLGGHAFCRNPDNDIRPWCFVLNRDRLSWEYCDLAQCQTPTQAAPPTPVSPRLHVPLMPAQPAPPKPQPTTRTPPQSQTPGALPAKREQPPSLTRNGPLSCGQRLRKSLSSMTR |
预测分子量 | 43.3 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F12重组蛋白的3篇参考文献示例(注:文献信息为虚构,仅用于示例):
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1. **文献名称**: *Expression and Functional Characterization of Recombinant Human Coagulation Factor XII in Mammalian Cells*
**作者**: Smith A, et al.
**摘要**: 研究通过哺乳动物表达系统成功制备重组人F12蛋白,并验证其与天然F12相似的酶活性及促凝功能,为研究凝血级联反应提供工具。
2. **文献名称**: *Structural Insights into Recombinant Factor XII Activation by Sulfatides*
**作者**: Tanaka K, et al.
**摘要**: 利用X射线晶体学解析重组F12蛋白与硫酸酯类物质结合的构象变化,揭示其激活机制及在病理性血栓形成中的潜在作用。
3. **文献名称**: *Recombinant Factor XII Deficiency Model for Studying Hereditary Angioedema Pathogenesis*
**作者**: Müller S, et al.
**摘要**: 通过基因编辑技术构建重组F12缺陷型小鼠模型,证明F12在缓激肽介导的血管性水肿中的调控作用,为疾病治疗提供新靶点。
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**备注**:实际文献需通过学术数据库(如PubMed、Web of Science)检索关键词“recombinant Factor XII”“F12 protein expression”等获取。建议结合具体研究方向筛选近年高相关性论文。
**Background of F12 Recombinant Protein**
The F12 recombinant protein is derived from human coagulation factor XII (FXII), a serine protease encoded by the *F12* gene on chromosome 5. FXII plays a dual role in hemostasis and inflammatory pathways. Initially identified as a key component of the intrinsic coagulation cascade, it is activated by contact with negatively charged surfaces (e.g., collagen, polyphosphates, or artificial materials) into its active form, FXIIa. This triggers a cascade leading to thrombin generation and fibrin clot formation. However, unlike other clotting factors, FXII deficiency is not linked to bleeding disorders, shifting research focus toward its involvement in pathological thrombosis and inflammation.
Recombinant F12 protein is produced using genetic engineering techniques, often expressed in mammalian cell systems (e.g., HEK293 or CHO cells) to ensure proper post-translational modifications. This allows large-scale production of highly purified, functional FXII for research and therapeutic development. Its recombinant form has been instrumental in studying contact activation pathways, thrombotic mechanisms, and crosstalk between coagulation and innate immunity.
Recent studies highlight FXII's role in diseases beyond coagulation, including hereditary angioedema, Alzheimer’s disease, and cancer metastasis. Recombinant F12 enables targeted exploration of these pathways and the development of inhibitors (e.g., anti-FXII antibodies or small molecules) as potential anticoagulants with reduced bleeding risks compared to traditional therapies. Additionally, it aids in evaluating biomaterial biocompatibility, as FXII activation on medical devices often drives clot formation.
Despite progress, challenges remain in understanding FXII's pleiotropic functions and optimizing recombinant variants for clinical use. Ongoing research aims to dissect its structure-activity relationships and refine therapeutic strategies targeting FXII in thrombosis and inflammatory disorders.
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