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Rabbit Polyclonal SCN1A Antibody

  • 中文名: SCN1A抗体
  • 别    名: FEB3; FHM3; NAC1; SCN1; SMEI; EIEE6; FEB3A; HBSCI; GEFSP2; Nav1.1
货号: IPDX04440
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

参考文献

以下是3篇关于SCN1A抗体的代表性文献,按研究领域分类整理:

1. **《Autoantibodies to epilepsy-related proteins in SCN1A-associated Dravet syndrome》**

- 作者:Ohashi, N., et al. (2021)

- 摘要:首次报道在部分Dravet综合征患者血清中检测到SCN1A抗体,提示自身免疫机制可能参与疾病表型异质性,但抗体致病性需进一步验证。

2. **《SCN1A antibody-mediated neuronal excitability in autoimmune encephalitis models》**

- 作者:Martínez-Hernández, E., et al. (2019)

- 摘要:通过体外培养神经元模型,证实抗SCN1A抗体可特异性结合钠通道,导致动作电位阈值升高,为抗体功能学研究提供实验依据。

3. **《Clinical spectrum of anti-SCN1A encephalitis: A multicenter cohort study》**

- 作者:Shi, Y., et al. (2022)

- 摘要:多中心研究揭示抗SCN1A脑炎患者以癫痫持续状态、认知减退为主要表现,部分患者对免疫治疗反应良好,提示该抗体可能作为新的诊断生物标志物。

注:上述文献为模拟范例,实际引用时建议通过PubMed/Google Scholar检索最新研究,关键词组合推荐:"SCN1A antibody" + "encephalitis"/"epilepsy"/"autoantibody"。部分重要研究可能发表于*Neurology*、*Epilepsia*等期刊。

背景信息

The SCN1A gene encodes the α1 subunit of the voltage-gated sodium channel Nav1.1. critical for neuronal excitability, particularly in inhibitory GABAergic interneurons. Antibodies targeting SCN1A or Nav1.1 are primarily studied in two contexts: autoimmune encephalitis and experimental research tools. In autoimmune neurology, anti-SCN1A antibodies are rare but identified in patients with encephalitis or epilepsy syndromes. These autoantibodies may disrupt Nav1.1 function, impairing inhibitory signaling and causing hyperexcitability, manifesting as seizures, cognitive deficits, or movement disorders. Their detection, often via cell-based assays, aids in diagnosing immune-mediated conditions, though clinical significance requires correlation with symptoms and treatment response. Experimentally, SCN1A-specific antibodies are used to study channel localization, function, and dysfunction in diseases like Dravet syndrome (caused by SCN1A mutations). Research highlights their dual role: pathogenic drivers in autoimmunity and investigative tools for channelopathies. Challenges include confirming pathogenicity and distinguishing them from cross-reactive antibodies. Immunotherapies (steroids, IVIg) may benefit seropositive patients, underscoring the importance of antibody characterization in guiding treatment.

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