| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 1/100-1/300 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Amiloride-sensitive sodium channel subunit beta; Beta-NaCH; Epithelial Na(+) channel subunit beta; Beta-ENaC; ENaCB; Nonvoltage-gated sodium channel 1 subunit beta; SCNEB |
| Entrez GeneID | 6338; |
| WB Predicted band size | 73kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse,Rat |
| Immunogen | KLH-conjugated synthetic peptide encompassing a sequence within the C-term region of human SCNN1B. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于 Beta-NaCH (phospho-Thr615) 抗体的模拟参考文献示例：
1. **"Phosphorylation of the Sodium Channel β1 Subunit at Thr615 Regulates Neuronal Excitability"**
*Authors: Smith A, et al.*
摘要：研究揭示了 β1 钠通道亚基 Thr615 磷酸化对神经元动作电位调控的作用，通过特异性抗体证实该修饰可增强通道失活，影响癫痫模型中的异常放电。
2. **"Development of a Phospho-Specific Antibody for Detecting β-NaCH Thr615 Phosphorylation in Cardiac Myocytes"**
*Authors: Chen L, et al.*
摘要：本文报道了一种高特异性抗体的制备与验证，用于检测心肌细胞中 β-NaCH Thr615 位点的磷酸化，并发现其在心力衰竭模型中磷酸化水平显著升高。
3. **"Kinase-Dependent Modulation of β-NaCH via Thr615 Phosphorylation in Neuropathic Pain"**
*Authors: Kimura R, et al.*
摘要：研究利用 phospho-Thr615 抗体证明，蛋白激酶 C(PKC)介导的 β-NaCH 磷酸化可增强背根神经节神经元兴奋性，促进慢性疼痛的发生。
4. **"Thr615 Phosphorylation of β-NaCH Subunit as a Biomarker for Arrhythmia Risk Assessment"**
*Authors: Gonzalez M, et al.*
摘要：通过临床样本分析，发现 β-NaCH Thr615 磷酸化水平与心律失常患者的心肌钠电流异常相关，提示该抗体在疾病诊断中的潜在应用价值。
(注：以上为模拟生成的参考文献，实际文献需通过学术数据库检索确认。)
The Beta-NaCh (phospho-Thr615) antibody is a specialized tool used to study phosphorylation of the voltage-gated sodium channel β1 subunit (SCN1B) at threonine 615 (Thr615). Sodium channels are critical for initiating and propagating action potentials in excitable cells. The β1 subunit, a regulatory component, modulates channel gating, cell adhesion, and interacts with cytoskeletal proteins. Phosphorylation at Thr615. located in the intracellular domain of β1. is implicated in post-translational regulation of sodium channel function, influencing membrane excitability and signaling pathways. This modification may be mediated by kinases such as protein kinase C (PKC) or Ca²⁺/calmodulin-dependent kinase II (CaMKII), linking cellular signaling to channel activity.
The Beta-NaCh (phospho-Thr615) antibody enables detection of this phosphorylation event via techniques like Western blotting, immunofluorescence, or immunoprecipitation. It is particularly valuable in studying conditions where sodium channel dysregulation occurs, including epilepsy, cardiac arrhythmias, neuropathic pain, and neurodegenerative diseases. Research using this antibody helps clarify how phosphorylation at Thr615 impacts channel trafficking, protein interactions, or pathological hyperexcitability. Validation typically includes testing in knockout models or phosphorylation-deficient mutants to ensure specificity. Understanding Thr615 phosphorylation may reveal therapeutic targets for diseases associated with sodium channel dysfunction.
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