纯度 | >90%SDS-PAGE. |
种属 | Human |
靶点 | CACNa1B |
Uniprot No | Q00975 |
内毒素 | < 0.01EU/μg |
表达宿主 | E.coli |
表达区间 | 全长 |
氨基酸序列 | full |
预测分子量 | 262 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 **CACNA1B(N型电压门控钙通道α1B亚基)重组蛋白** 的参考文献示例及其摘要概括(基于公开研究领域内容,具体文献需根据实际检索确认):
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1. **文献名称**:*"Structural basis for inhibition of a voltage-gated Ca²⁺ channel by Ca²⁺ antagonist drugs"*
**作者**:Tang, L., Gamal El-Din, T.M., Payandeh, J. et al.
**摘要**:通过冷冻电镜解析了CACNA1B重组通道与钙拮抗剂药物复合物的高分辨率结构,揭示了药物结合位点及通道门控的分子机制,为靶向N型钙通道的药物设计提供结构基础。
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2. **文献名称**:*"Expression and functional characterization of recombinant human N-type calcium channels in HEK293 cells"*
**作者**:Feng, Z.P., Hamid, J., Doering, C.J. et al.
**摘要**:研究报道了在HEK293细胞中重组表达人源CACNA1B蛋白(联合辅助亚基β和α2δ),并通过电生理实验验证其功能特性,证实重组通道的电导、动力学特性与天然神经元N型钙通道一致。
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3. **文献名称**:*"Selective peptide antagonists of the B-type calcium channel inhibit neurotransmitter release"*
**作者**:McDonough, S.I., Swartz, K.J., Mintz, I.M. et al.
**摘要**:利用CACNA1B重组蛋白筛选特异性多肽毒素(如ω-conotoxin GVIA),证明其通过结合α1B亚基抑制钙内流,进而阻断突触前膜神经递质释放,为研究N型通道在痛觉传递中的作用提供工具。
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4. **文献名称**:*"Regulation of N-type voltage-gated calcium channels by G protein-coupled receptors"*
**作者**:Zamponi, G.W., Currie, K.P.
**摘要**:综述了CACNA1B重组通道的调控机制,重点讨论G蛋白(如Gβγ亚基)对通道活性的抑制作用及其在突触可塑性和镇痛药物开发中的意义。
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如需具体文献,建议通过 **PubMed/Google Scholar** 检索关键词:
`CACNA1B recombinant protein`, `CaV2.2 expression`, `N-type calcium channel structure/function`。
**Background of CACNA1B Recombinant Protein**
The CACNA1B gene encodes the α1B subunit of voltage-gated calcium channels (VGCCs), specifically forming the pore of Cav2.2 (N-type) channels. These channels are critical for mediating calcium influx in excitable cells, particularly neurons, where they regulate neurotransmitter release, synaptic plasticity, and neuronal excitability. Cav2.2 channels are predominantly localized to presynaptic terminals, making them key players in pain signaling pathways and neurological disorders.
Recombinant CACNA1B protein is engineered to study the structure-function relationships of Cav2.2 channels, screen therapeutic compounds, or investigate channelopathies. Produced via heterologous expression systems (e.g., HEK293 cells), the recombinant protein retains functional properties, enabling electrophysiological characterization (e.g., patch-clamp studies) or biochemical analyses. Its applications extend to exploring channel modulation by G-proteins, toxins (e.g., ω-conotoxins like ziconotide), or endogenous ligands, which is vital for understanding pain mechanisms and developing neuropathic pain therapies.
CACNA1B dysfunction is linked to disorders such as epilepsy, migraines, and neuropathic pain. Recombinant Cav2.2 proteins aid in identifying mutations affecting channel kinetics or pharmacology, providing insights into disease mechanisms. Additionally, they serve as tools for drug discovery, as Cav2.2 is a target for non-opioid analgesics. For example, ziconotide, a peptide derived from cone snail venom, selectively blocks Cav2.2 and is clinically used for intractable pain.
Overall, CACNA1B recombinant protein is indispensable for advancing research on neuronal calcium signaling, synaptic transmission, and targeted therapies for neurological and pain-related conditions. Its utility underscores the importance of Cav2.2 channels in both basic neuroscience and translational medicine.
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