| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | CPLX2 |
| Uniprot No | Q6PUV4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-134aa |
| 氨基酸序列 | MDFVMKQALGGATKDMGKMLGGEEEKDPDAQKKEEERQEALRQQEEERKAKHARMEAEREKVRQQIRDKYGLKKKEEKEAEEKAALEQPCEGSLTRPKKAIPAGCGDEEEEEEESILDTVLKYLPGPLQDMFKK |
| 预测分子量 | 42.4kDa |
| 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CPLX2重组蛋白的3篇代表性文献的简要总结(注：文献为虚拟示例，实际文献需根据数据库检索)：
1. **文献名称**: "Recombinant CPLX2 expression and its role in synaptic vesicle regulation"
**作者**: Smith A, et al.
**摘要**: 本研究在大肠杆菌系统中成功表达并纯化了重组CPLX2蛋白，验证其与SNARE复合物的相互作用。实验表明，重组CPLX2通过抑制突触小泡过早融合，调控神经递质释放的精确性。
2. **文献名称**: "Structural analysis of human CPLX2 using recombinant protein technology"
**作者**: Lee B, et al.
**摘要**: 通过哺乳动物细胞表达系统获得高纯度人源CPLX2重组蛋白，结合X射线晶体学解析其三维结构，揭示了其C端结构域在钙离子依赖性膜融合中的关键功能位点。
3. **文献名称**: "CPLX2 recombinant protein rescues synaptic dysfunction in murine models"
**作者**: García-Ramos C, et al.
**摘要**: 利用杆状病毒-昆虫细胞系统规模化生产功能性CPLX2重组蛋白。动物实验证实，外源性CPLX2可改善阿尔茨海默病模型小鼠的突触传递缺陷，为神经退行性疾病治疗提供新思路。
*提示：实际研究中建议通过PubMed/Google Scholar以"CPLX2 recombinant protein"为关键词检索最新文献，重点关注蛋白表达策略(原核/真核系统)、功能机制研究或疾病相关应用方向。*
CPLX2 (Complexin 2) is a synaptic protein critical for regulating neurotransmitter release in the nervous system. As a member of the complexin family, it functions as a key modulator of synaptic vesicle fusion, working in tandem with the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex. CPLX2 stabilizes the pre-fusion state of synaptic vesicles, preventing spontaneous exocytosis while simultaneously enhancing calcium-triggered synchronous release. This dual role ensures precise control over synaptic transmission, maintaining the balance between signal fidelity and responsiveness.
Expressed predominantly in the central nervous system, CPLX2 is enriched in neurons of the hippocampus, cortex, and cerebellum, regions associated with learning, memory, and motor coordination. Its activity is tightly linked to synaptic plasticity, a cellular basis for information processing and adaptation. Studies using knockout models reveal that CPLX2 deficiency disrupts synaptic vesicle pool organization, leading to impaired neurotransmitter release and altered neural circuit dynamics. These findings underscore its importance in maintaining normal cognitive and behavioral functions.
The recombinant CPLX2 protein, produced via heterologous expression systems (e.g., E. coli or mammalian cells), retains the native structure and functional domains necessary for biochemical studies. Researchers employ it to investigate synaptic mechanisms, screen potential neuroactive compounds, or develop diagnostics for neurological disorders. Notably, altered CPLX2 expression has been implicated in neuropsychiatric conditions such as schizophrenia and autism spectrum disorders, making it a biomarker candidate and therapeutic target. Its conserved N-terminal domain and central α-helical region are particularly scrutinized for their roles in membrane interactions and SNARE complex regulation.
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