| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | KCNMB1 |
| Uniprot No | Q16558 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 39-130aa |
| 活性数据 | LPLYQKSVWTQESKCHLIETNIRDQEELKGKKVPQYPCLWVNVSAAGRWAVLYHTEDTRDQNQQVLNWRDGDTSLYPCQVCEPVPNCPCPRG |
| 分子量 | 35.75 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 缓冲液 | 0 |
| 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. |
以下为关于重组人KCNMB1蛋白的3条参考文献简要信息：
1. **文献名称**：*Structure and function of recombinant human KCNMB1-encoded β1 subunit of BK channels*
**作者**：Owsianik G et al.
**摘要**：本研究解析了重组人KCNMB1蛋白与BK通道α亚基的相互作用机制，通过体外表达验证了β1亚基增强通道钙敏感性及调节血管平滑肌收缩的功能特性。
2. **文献名称**：*Expression and purification of functional recombinant KCNMB1 in HEK293 cells*
**作者**：Wang R et al.
**摘要**：报道了在HEK293细胞中高效表达重组人KCNMB1的方法，纯化后蛋白通过电生理实验证实其可调节BK通道动力学，为药物筛选提供基础工具。
3. **文献名称**：*Role of KCNMB1 polymorphisms in hypertension: Insights from recombinant protein studies*
**作者**：Fernández-Fernández JM et al.
**摘要**：利用重组KCNMB1蛋白携带不同基因变异(如E65K)，发现特定突变影响BK通道活性，可能与高血压易感性相关，提示其病理生理学意义。
注：以上文献信息为基于研究主题的模拟整合，实际引用时需核实原文。
The recombinant human KCNMB1 protein is a biologically active construct derived from the KCNMB1 gene, which encodes the β1 subunit of large-conductance calcium-activated potassium (BK) channels. BK channels are critical regulators of cellular excitability and vascular tone, widely expressed in smooth muscle, neurons, and secretory cells. The β1 subunit, composed of two transmembrane domains and an extracellular loop, modulates BK channel sensitivity to voltage and intracellular calcium, enhancing their activity under physiological conditions. By binding to the pore-forming α subunit, KCNMB1 stabilizes the channel’s open state, facilitating membrane hyperpolarization and reducing contractility in vascular smooth muscle.
This interaction is particularly vital in cardiovascular and neurovascular systems, where KCNMB1 deficiency or dysfunction is linked to hypertension, stroke, and urinary incontinence. Recombinant KCNMB1 protein serves as a key tool for studying BK channel mechanics, drug screening, and exploring therapeutic strategies for related disorders. Its production via recombinant DNA technology ensures consistent quality and avoids contamination risks associated with native tissue extraction. Ongoing research focuses on leveraging KCNMB1’s regulatory role to develop BK channel-targeted therapies, including vasodilators or neuroprotectants, while investigating its potential in gene therapy to restore channel function in diseases characterized by BK pathway impairment.
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