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Rabbit Polyclonal SCN9A Antibody

  • 中文名: SCN9A抗体
  • 别    名: PN1; ETHA; NENA; SFNP; FEB3B; NE-NA; GEFSP7; Nav1.7
货号: IPDX11336
Price: ¥1180
数量:
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验证与应用

应用及物种
WB 咨询技术 Human,Mouse,Rat
IF 咨询技术 Human,Mouse,Rat
IHC 1/50-1/200 Human,Mouse,Rat
ICC 技术咨询 Human,Mouse,Rat
FCM 咨询技术 Human,Mouse,Rat
Elisa 1/2000-1/5000 Human,Mouse,Rat

产品详情

AliasesPN1; ETHA; NENA; SFNP; FEB3B; NE-NA; GEFSP7; Nav1.7
Host/IsotypeRabbit IgG
Antibody TypePrimary antibody
StorageStore at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.
Species ReactivityHuman
ImmunogenSynthetic peptide of human SCN9A
FormulationPurified antibody in PBS with 0.05% sodium azide and 50% glycerol.

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参考文献

以下是关于SCN9A抗体的示例参考文献(注:以下内容为模拟示例,实际文献需通过学术数据库核实):

1. **文献名称**: *"Selective Nav1.7 Blockade with a Monoclonal Antibody Attenuates Nociceptive Signaling in Pain Pathways"*

**作者**: Smith J, Doe R, Brown K

**摘要**: 本研究开发了一种靶向SCN9A编码的Nav1.7通道的单克隆抗体,通过抑制其活性显著降低动物模型的炎性和神经性疼痛反应,证明其作为新型镇痛疗法的潜力。

2. **文献名称**: *"Characterization of SCN9A Expression in Human Dorsal Root Ganglia Using a Novel Polyclonal Antibody"*

**作者**: Zhang L, Dib-Hajj SD, Waxman SG

**摘要**: 通过新开发的多克隆抗体进行免疫组化和Western blot分析,揭示SCN9A/Nav1.7在人类背根神经节中的特异性分布,支持其在痛觉神经元中的关键作用。

3. **文献名称**: *"Anti-SCN9A Antibodies as Biomarkers in Autoimmune Small Fiber Neuropathy"*

**作者**: Garcia-Castro M, et al.

**摘要**: 研究发现部分自身免疫性小纤维神经病变患者血清中存在抗SCN9A抗体,提示其可能通过干扰Nav1.7功能导致疼痛异常,为疾病诊断提供新标志物。

4. **文献名称**: *"Functional Validation of SCN9A Variants Using Antibody-Based Protein Quantification"*

**作者**: Lee H, Yang X, Patel PN

**摘要**: 结合SCN9A特异性抗体与质谱技术,定量分析基因突变对Nav1.7蛋白表达的影响,为遗传性疼痛综合征的机制研究提供方法学支持。

建议通过PubMed或Google Scholar搜索关键词“SCN9A antibody”、“Nav1.7 therapeutic antibody”获取最新文献。

背景信息

SCN9A antibodies target the protein product of the SCN9A gene, which encodes the alpha subunit of the voltage-gated sodium channel Nav1.7. This channel is predominantly expressed in peripheral sensory and sympathetic neurons, where it plays a critical role in action potential generation and propagation. Nav1.7 is a key mediator of pain signaling, and mutations in SCN9A are linked to inherited pain disorders such as primary erythromelalgia (gain-of-function mutations) and congenital insensitivity to pain (loss-of-function mutations). Researchers utilize SCN9A-specific antibodies to study the expression, localization, and functional regulation of Nav1.7 in both physiological and pathological contexts. These antibodies are essential tools for immunohistochemistry, Western blotting, and cellular imaging, enabling investigations into channel dysfunction mechanisms underlying neuropathic pain, small fiber neuropathy, and other sodium channelopathies. Additionally, they support drug discovery efforts aimed at developing Nav1.7-targeted analgesics, which hold promise for treating chronic pain with reduced side effects compared to conventional opioids. The specificity and validation of SCN9A antibodies are crucial, as cross-reactivity with other sodium channel isoforms (e.g., Nav1.8. Nav1.9) could lead to misleading results in complex tissues like dorsal root ganglia. Ongoing research continues to refine antibody-based methodologies to better understand Nav1.7's role in pain pathways and its therapeutic potential.

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