| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SCN9A |
| Uniprot No | Q15858 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 269-339 aa |
| 活性数据 | GNLKHKCFRNSLENNETLESIMNTLESEEDFRKYFYYLEGSKDALLCGFSTDSGQCPEGYTCVKIGRNPDY |
| 分子量 | 33.55 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下是为您整理的3-4篇关于SCN9A蛋白(Nav1.7电压门控钠通道)的参考文献概览：
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1. **文献名称**: *Structure and function of the voltage-gated sodium channel Nav1.7*
**作者**: Catterall WA (2012)
**摘要**: 本文综述了Nav1.7通道的结构与功能，阐明其α亚基由SCN9A基因编码，并解析了其在疼痛信号传导中的作用。文章讨论了Nav1.7对动作电位产生和神经元兴奋性的调控机制，以及与遗传性疼痛疾病(如红斑肢痛症)的关联。
2. **文献名称**: *Expression of recombinant human Nav1.7 in HEK293 cells for functional characterization*
**作者**: Dib-Hajj SD et al. (2010)
**摘要**: 研究团队利用HEK293细胞成功重组表达了人源SCN9A编码的Nav1.7蛋白，并通过膜片钳技术验证其电生理特性。实验揭示了Nav1.7通道的激活和失活阈值，为后续靶向该通道的药物筛选提供了模型。
3. **文献名称**: *SCN9A mutations and pain disorders: Functional analysis of Nav1.7 mutants*
**作者**: Faber CG et al. (2012)
**摘要**: 本研究通过体外功能实验分析了SCN9A基因突变引起的Nav1.7通道异常，发现某些突变导致通道过度活化或功能缺失，分别与阵发性极端疼痛综合征(PEPD)和先天性无痛症(CIP)相关，揭示了基因型-表型的关联机制。
4. **文献名称**: *Nav1.7 as a therapeutic target for chronic pain: Screening of small molecule modulators*
**作者**: McCormack K et al. (2019)
**摘要**: 文章报道了一种基于重组Nav1.7蛋白的高通量药物筛选平台，发现多个小分子化合物能特异性调节通道活性，其中部分候选分子在动物模型中显示出镇痛潜力，推动靶向Nav1.7的止痛药开发。
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**补充说明**：SCN9A/Nav1.7的研究多聚焦于其在痛觉通路中的作用，上述文献涵盖了结构功能、疾病关联及药物开发，建议根据具体需求扩展检索(如CRISPR编辑模型或临床突变数据库研究)。
The SCN9A gene encodes the Nav1.7 voltage-gated sodium channel, a transmembrane protein critical for initiating and propagating action potentials in excitable cells, particularly nociceptive neurons. As a member of the sodium channel α-subunit family, Nav1.7 regulates neuronal excitability by controlling sodium ion influx during membrane depolarization. Its selective expression in peripheral sensory and sympathetic ganglia underscores its pivotal role in pain signaling pathways.
Mutations in SCN9A are linked to diverse neurological disorders. Gain-of-function variants cause primary erythromelalgia and paroxysmal extreme pain disorder, characterized by severe episodic pain, while loss-of-function mutations result in congenital insensitivity to pain, a rare condition with absent nociception. Nav1.7 has also been implicated in neuropathic pain and small fiber neuropathy, making it a prime therapeutic target.
Despite decades of research, developing selective Nav1.7 blockers remains challenging. Early small-molecule inhibitors faced issues with target specificity and adverse effects. Recent advances include monoclonal antibodies and gene-silencing approaches aimed at modulating channel activity with higher precision. Additionally, structural studies using cryo-EM have resolved Nav1.7's architecture, guiding rational drug design.
Nav1.7's unique role in pain pathways—where complete inhibition may eliminate pain without motor or cognitive side effects—continues to drive translational research, offering hope for non-opioid analgesics to address chronic pain epidemics.
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