| 纯度 | > 90 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | CCM2 |
| Uniprot No | Q9BSQ5-3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 66-353aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSEVKYLGQLTSIPGYLNPSSRTEILHFI DNAKRAHQLPGHLTQEHDAVLSLSAYNVKLAWRDGEDIILRVPIHDIAAV SYVRDDAAHLVVLKTDDSSTKVDIKETYEVEASTFCFPESVDVGGASPHS KTISESELSASATELLQDYMLTLRTKLSSQEIQQFAALLHEYRNGASIHE FCINLRQLYGDSRKFLLLGLRPFIPEKDSQHFENFLETIGVKDGRGIITD SFGRHRRALSTTSSSTTNGNRATGSSDDRSAPSEGDEWDRMISDISSDIE ALGCSMDQDSA |
| 预测分子量 | 34 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CCM2重组蛋白的3篇虚构参考文献示例，结构符合学术文献格式，供参考：
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1. **文献名称**: *Expression and Functional Analysis of Recombinant CCM2 Protein in Vascular Endothelial Cells*
**作者**: Smith J, Lee R, Chen W
**摘要**: 本研究通过大肠杆菌表达系统成功纯化CCM2重组蛋白，并验证其与KRIT1的结合能力。实验表明，重组CCM2蛋白可通过调控RhoA/ROCK信号通路抑制内皮细胞迁移，为CCM疾病的分子机制研究提供了工具。
2. **文献名称**: *Structural Insights into CCM2-OSM Interaction Using Recombinant Protein Complexes*
**作者**: García M, Park S, Müller T
**摘要**: 通过X射线晶体学解析CCM2重组蛋白与OSM的复合物结构，揭示两者结合的关键结构域。体外实验证实，重组CCM2缺失突变体无法维持血管内皮屏障稳定性，突显其结构对功能的重要性。
3. **文献名称**: *High-Throughput Screening of CCM2-Binding Compounds Using Purified Recombinant Protein*
**作者**: Kim H, Zhang L, O'Connor B
**摘要**: 利用亲和层析纯化的CCM2重组蛋白建立药物筛选平台，鉴定出3种小分子可增强CCM2与KRIT1的互作。该研究为靶向CCM复合体的治疗策略开发提供了实验基础。
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注：以上文献为虚构内容，仅用于示例。实际研究中请通过PubMed、Web of Science等数据库检索真实文献。
The CCM2 (Cerebral Cavernous Malformation 2) recombinant protein is derived from the human CCM2 gene, which encodes a critical scaffold protein involved in vascular development and homeostasis. CCM2. also known as Malcavernin or OSM, forms a ternary complex with CCM1 (KRIT1) and CCM3 (PDCD10) to regulate endothelial cell function, blood vessel stability, and angiogenesis. This complex primarily modulates signaling pathways like Rho/ROCK and MEKK3-ERK, which govern cell-cell adhesion, cytoskeletal organization, and vascular permeability.
Mutations in CCM2 are linked to cerebral cavernous malformations (CCMs), a neurovascular disorder characterized by fragile, leaky blood vessels in the brain that predispose individuals to seizures, hemorrhages, and neurological deficits. Recombinant CCM2 protein is engineered using expression systems (e.g., E. coli, mammalian cells) to study its molecular interactions, structural domains (e.g., PTB domain for binding CCM1), and pathogenic mechanisms. Researchers utilize it to investigate loss-of-function effects, pathway dysregulation, and potential therapeutic targets.
The recombinant protein is purified via affinity tags (e.g., His-tag, GST-tag) and validated for functional assays, including protein-protein interaction studies, endothelial cell migration assays, and in vitro angiogenesis models. Its applications extend to drug screening for CCMs, mechanistic studies of vascular biology, and developing gene therapies. By dissecting CCM2's role in maintaining vascular integrity, this tool advances understanding of cerebrovascular diseases and informs strategies to restore normal signaling in CCM-associated pathologies.
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