| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | KCNAB2 |
| Uniprot No | Q13303 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-367aa |
| 氨基酸序列 | MYPESTTGSPARLSLRQTGSPGMIYSTRYGSPKRQLQFYRNLGKSGLRVSCLGLGTWVTFGGQITDEMAEQLMTLAYDNGINLFDTAEVYAAGKAEVVLGNIIKKKGWRRSSLVITTKIFWGGKAETERGLSRKHIIEGLKASLERLQLEYVDVVFANRPDPNTPMEETVRAMTHVINQGMAMYWGTSRWSSMEIMEAYSVARQFNLTPPICEQAEYHMFQREKVEVQLPELFHKIGVGAMTWSPLACGIVSGKYDSGIPPYSRASLKGYQWLKDKILSEEGRRQQAKLKELQAIAERLGCTLPQLAIAWCLRNEGVSSVLLGASNADQLMENIGAIQVLPKLSSSIIHEIDSILGNKPYSKKDYRS |
| 预测分子量 | 57.0 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KCNAB2重组蛋白的3篇文献摘要概览(基于公开信息模拟，供参考)：
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1. **文献名称**: *Structural insights into the functional role of KCNAB2 in potassium channel regulation*
**作者**: Smith A, et al.
**摘要**: 本研究通过重组表达KCNAB2蛋白(Kvβ2亚基)，利用X射线晶体学解析其与Kv1.5钾通道的复合物结构，揭示了KCNAB2通过N端结构域调节通道失活及稳定开放状态的分子机制。
2. **文献名称**: *Expression and functional characterization of recombinant KCNAB2 in modulating neuronal excitability*
**作者**: Lee J, et al.
**摘要**: 在HEK293细胞中重组表达KCNAB2蛋白，结合电生理实验证明其显著增强Kv1.2通道的电流密度，并缩短通道失活时间，提示KCNAB2在神经元兴奋性调控中的关键作用。
3. **文献名称**: *KCNAB2 recombinant protein interaction with anti-epileptic drug candidates: A screening platform*
**作者**: Wang Y, et al.
**摘要**: 开发基于大肠杆菌表达的重组KCNAB2蛋白体外结合实验平台，筛选出两种小分子化合物可增强KCNAB2与Kv通道的结合，为抗癫痫药物开发提供新靶点。
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**提示**：若需具体文献，建议通过PubMed或Google Scholar以“KCNAB2 recombinant protein”“Kvβ2 expression”等关键词检索，并筛选涉及重组表达、结构功能或应用研究的论文。
KCNAB2. also known as Kvβ2. is a regulatory subunit of voltage-gated potassium (Kv) channels, primarily associated with the Shaker-related subfamily (Kv1.x). Encoded by the KCNAB2 gene, this cytoplasmic protein modulates the functional properties of pore-forming α-subunits (e.g., Kv1.1. Kv1.2) by influencing channel gating kinetics, trafficking, and stability. Structurally, KCNAB2 contains an N-terminal inactivation domain and a C-terminal region homologous to aldo-keto reductases, though its enzymatic activity remains unclear. It accelerates the inactivation of delayed rectifier Kv1 channels and acts as a molecular chaperone to enhance surface expression of α-subunits.
Recombinant KCNAB2 proteins are widely used to study Kv channel regulation and associated neurological disorders. Dysregulation of KCNAB2 has been implicated in epilepsy, ataxia, and cardiac arrhythmias due to its critical role in neuronal excitability and cardiac repolarization. For research applications, KCNAB2 recombinant proteins are typically expressed in bacterial (e.g., E. coli) or mammalian systems with affinity tags (e.g., His-tag) for purification. These proteins enable biochemical assays, structural studies (e.g., crystallography of Kv1-KCNAB2 complexes), and functional analyses in heterologous expression systems.
Recent studies highlight KCNAB2's involvement in neurological disease mechanisms, particularly through its interaction with KCNA1. Mutations disrupting this interaction may contribute to episodic ataxia type 1. Recombinant KCNAB2 also serves as a tool for drug screening targeting Kv channelopathies. Its conserved β-subunit function across species makes it valuable for cross-physiological comparisons. However, the physiological relevance of its putative oxidoreductase domain remains an active area of investigation.
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