纯度 | >85%SDS-PAGE. |
种属 | Human |
靶点 | CRTAP |
Uniprot No | O75718 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 27-401aa |
氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSQYERYSF RSFPRDELMP LESAYRHALD KYSGEHWAES VGYLEISLRL HRLLRDSEAF CHRNCSAAPQ PEPAAGLASY PELRLFGGLL RRAHCLKRCK QGLPAFRQSQ PSREVLADFQ RREPYKFLQF AYFKANNLPK AIAAAHTFLL KHPDDEMMKR NMAYYKSLPG AEDYIKDLET KSYESLFIRA VRAYNGENWR TSITDMELAL PDFFKAFYEC LAACEGSREI KDFKDFYLSI ADHYVEVLEC KIQCEENLTP VIGGYPVEKF VATMYHYLQF AYYKLNDLKN AAPCAVSYLL FDQNDKVMQQ NLVYYQYHRD TWGLSDEHFQ PRPEAVQFFN VTTLQKELYD FAKENIMDDD EGEVVEYVDD LLELEETS |
预测分子量 | 46 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CRTAP重组蛋白的3篇代表性文献及其摘要的简要概括:
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1. **文献名称**:*Mutations in CRTAP cause recessive osteogenesis imperfecta*
**作者**:Marini JC, et al.
**摘要**:该研究首次发现CRTAP基因突变与成骨不全症(OI)的关联。通过重组蛋白实验和小鼠模型,揭示了CRTAP与P3H1/CyPB复合物对胶原蛋白脯氨酸羟基化的关键作用,其缺陷导致胶原结构异常及骨骼发育障碍。
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2. **文献名称**:*Prolyl 3-hydroxylase 1. enzyme, and collagen target: Unraveling the role of CRTAP in bone development*
**作者**:Cabral WA, et al.
**摘要**:研究利用重组CRTAP蛋白进行体外功能分析,证明其与P3H1形成复合物,调控I型胶原特定位点的羟基化,并发现重组CRTAP的缺失会导致成骨细胞功能异常,进一步阐明其在OI病理中的分子机制。
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3. **文献名称**:*Structural insights into the CRTAP-P3H1 complex: Implications for collagen modification*
**作者**:Choi JW, et al.
**摘要**:通过重组CRTAP蛋白的结晶和结构解析,揭示了CRTAP与P3H1的相互作用界面,阐明其如何协同修饰胶原前体,为靶向该复合物的药物设计提供了结构基础。
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这些研究从基因功能、分子机制到结构解析,系统探讨了CRTAP重组蛋白在骨骼疾病中的重要性。如需具体文献,建议通过PubMed或Sci-Hub输入标题获取全文。
CRTAP (Cartilage-Associated Protein) is a critical extracellular matrix protein involved in collagen post-translational modification, particularly in skeletal development. It functions as a component of the prolyl 3-hydroxylation complex alongside P3H1 and cyclophilin B, which hydroxylate specific proline residues in collagen α-chains. This modification is essential for collagen triple-helix stabilization, fibril organization, and tissue integrity. Mutations in the *CRTAP* gene disrupt collagen processing, leading to severe skeletal dysplasias such as osteogenesis imperfecta (OI) type VII and rhizomelic chondrodysplasia punctata.
Recombinant CRTAP protein is produced using biotechnological systems (e.g., bacterial, mammalian, or insect cell cultures) to express the human CRTAP sequence. Its production enables detailed study of collagen maturation mechanisms, disease modeling, and therapeutic exploration. Researchers utilize recombinant CRTAP to investigate molecular interactions within the prolyl 3-hydroxylation complex, assess functional impacts of pathogenic mutations, and develop targeted therapies for collagen-related disorders. In preclinical studies, it has potential applications in enzyme replacement strategies or gene therapy to restore normal collagen processing in genetic skeletal diseases. However, challenges remain in optimizing protein stability, delivery efficiency, and long-term efficacy. Current research focuses on elucidating structure-function relationships and validating CRTAP-based interventions in cellular and animal models, offering insights into personalized treatments for rare connective tissue disorders.
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