| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | Phospholemman, FXYD domain-containing ion transport regulator 1, Fxyd1, Plm |
| Entrez GeneID | 56188 |
| WB Predicted band size | 10.3kDa |
| Host/Isotype | Mouse IgG1 |
| 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 | Mouse |
| Immunogen | This PLM Antibody is generated from mice immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S68 of mouse PLM. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于 **Phospho-PLM(S68) 抗体** 的参考文献示例(内容基于典型研究领域，部分信息可能需进一步验证)：
1. **"Phospholemman phosphorylation regulates cardiac Na+/K+-ATPase activity"**
- **作者**: Bossuyt, J., et al.
- **摘要**: 研究报道了PLM在S68位点的磷酸化通过调节钠钾泵(Na+/K+-ATPase)活性影响心脏功能，使用Phospho-PLM(S68)抗体在缺血再灌注模型中证实磷酸化水平升高与心律失常相关。
2. **"Ischemia-induced phosphorylation of phospholemman accelerates cardiac arrhythmias"**
- **作者**: Silverman, M.G., et al.
- **摘要**: 通过该抗体检测到心肌缺血时PLM(S68)磷酸化增强，揭示了其通过增加细胞内钠离子浓度加剧心律失常的机制。
3. **"Role of phospholemman S68 phosphorylation in heart failure progression"**
- **作者**: Han, F., et al.
- **摘要**: 在心力衰竭动物模型中，利用该抗体发现PLM(S68)磷酸化水平与心肌肥厚和收缩功能障碍呈正相关，提示其作为治疗靶点的潜力。
4. **"Antibody-specific detection of phospholemman phospho-isoforms in disease models"**
- **作者**: Fraser, J.A., et al.
- **摘要**: 评估了Phospho-PLM(S68)抗体的特异性，并应用于多种病理模型(如高血压、糖尿病心脏病变)，证明其在检测疾病相关磷酸化信号中的可靠性。
建议通过 **PubMed** 或 **Google Scholar** 检索具体文献标题和DOI以获取全文。
The Phospho-PLM(S68) antibody is a specialized tool used to detect phosphorylated phospholemman (PLM) at serine 68. a key post-translational modification involved in cardiac ion regulation. PLM, a small transmembrane protein encoded by the FXYD1 gene, primarily regulates the activity of the Na+/K+-ATPase (NKA) pump and the Na+/Ca2+ exchanger (NCX) in cardiac myocytes. Its phosphorylation at Ser68. mediated by protein kinase A (PKA) or protein kinase C (PKC), modulates NKA function by relieving inhibitory effects, thereby influencing intracellular sodium and calcium homeostasis. This process is critical for maintaining proper cardiac contractility and electrical stability.
The Phospho-PLM(S68) antibody is widely utilized in cardiovascular research to study PLM’s regulatory role in heart failure, arrhythmias, and ischemia-reperfusion injury. Elevated PLM phosphorylation at Ser68 has been linked to enhanced NKA activity under stress conditions, while dysregulation may contribute to pathological cardiac remodeling. Researchers employ this antibody in techniques like Western blotting, immunofluorescence, and immunohistochemistry to assess phosphorylation status in experimental models, providing insights into disease mechanisms and potential therapeutic targets. Its specificity for the phosphorylated Ser68 epitope makes it valuable for distinguishing active PLM signaling from its unmodified state.
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