| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | PRRT2 |
| Uniprot No | Q7Z6L0-3 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-268aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSMAASSSEISEMKGVEESPKVPGEGPGH SEAETGPPQVLAGVPDQPEAPQPGPNTTAAPVDSGPKAGLAPETTETPAG ASETAQATDLSLSPGGESKANCSPEDPCQETVSKPEVSKEATADQGSRLE SAAPPEPAPEPAPQPDPRPDSQPTPKPALQPELPTQEDPTPEILSESVGE KQENGAVVPLQAGDGEEGPAPEPHSPPSKKSPPANGAPPRVLQQLVEEDR MRRAHSGHPGSPRGSLSRHPSSQLAGPGVEGGEGTQKPRDY |
| 预测分子量 | 30 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PRRT2重组蛋白的3篇代表性文献(基于领域内常见研究方向整理，非真实文献，仅供参考)：
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1. **文献名称**：*PRRT2 interacts with SNAP25 to modulate synaptic vesicle exocytosis*
**作者**：Chen WJ, et al.
**摘要**：通过重组PRRT2蛋白的体外结合实验，发现其N端结构域直接与突触蛋白SNAP25结合，调控神经递质释放。研究揭示了PRRT2在突触可塑性中的分子机制，突变可能导致癫痫或运动障碍。
2. **文献名称**：*Crystal structure of human PRRT2 reveals a proline-rich domain critical for function*
**作者**：Ebrahimi-Fakhari D, et al.
**摘要**：首次解析了PRRT2重组蛋白的晶体结构，发现其富含脯氨酸的结构域对结合突触蛋白STX1A至关重要，为理解PRRT2突变相关疾病的致病机制提供结构基础。
3. **文献名称**：*PRRT2 regulates neuronal excitability via voltage-gated sodium channels*
**作者**：Lee HY, et al.
**摘要**：利用重组PRRT2蛋白进行功能研究，发现其通过调控钠离子通道Nav1.2的活性影响神经元兴奋性，为阵发性运动诱发性运动障碍(PKD)的病理机制提供了新视角。
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**注**：以上文献为模拟示例，实际研究需通过学术数据库(如PubMed、Google Scholar)以“PRRT2 recombinant protein”“PRRT2 structure/function”等关键词检索近年发表的论文。
PRRT2 (proline-rich transmembrane protein 2) is a gene encoding a neuronal protein predominantly expressed in the central nervous system, particularly in synapses. It plays a critical role in regulating synaptic transmission, neurotransmitter release, and neuronal excitability. PRRT2 mutations are linked to paroxysmal neurological disorders, including paroxysmal kinesigenic dyskinesia (PKD), benign familial infantile epilepsy (BFIE), and infantile convulsions with choreoathetosis (ICCA syndrome). These mutations often result in truncated or dysfunctional proteins, disrupting interactions with synaptic partners like SNAP25 and voltage-gated sodium channels, ultimately leading to hyperexcitability in neural circuits.
Recombinant PRRT2 protein is engineered in vitro using expression systems (e.g., bacterial, mammalian, or insect cells) to produce purified, functional protein for mechanistic studies. Its production enables researchers to investigate PRRT2’s structure-function relationships, post-translational modifications, and binding dynamics with synaptic proteins. For example, studies using recombinant PRRT2 have clarified its role in modulating Naᵥ1.2 sodium channel inactivation and synaptic vesicle fusion. Additionally, it serves as an antigen for antibody development or a substrate for high-throughput drug screening to identify compounds that restore PRRT2 function in mutation-associated disorders. Recent advances in cryo-EM and structural biology further utilize recombinant PRRT2 to resolve its conformational states, informing therapeutic strategies for paroxysmal neurological conditions. Ongoing research focuses on leveraging this tool to decode disease mechanisms and develop targeted interventions.
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