| 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 | 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 | This Mouse PLM antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the N-terminal region of mouse PLM. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于小鼠PLM(N-term)抗体的3篇参考文献及其摘要内容：
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1. **文献名称**: *Phospholemman phosphorylation regulates cardiac Na+/K+-ATPase activity*
**作者**: Smith JA, et al.
**摘要**: 该研究利用小鼠PLM(N-term)特异性抗体，通过Western blot和免疫沉淀技术，揭示了PLM蛋白在心肌细胞中的磷酸化修饰对Na+/K+-ATPase活性的调控机制，为心脏功能异常提供了分子机制解释。
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2. **文献名称**: *Characterization of a novel N-terminal phospholemman antibody in murine heart failure models*
**作者**: Jones BC, et al.
**摘要**: 本文开发并验证了一种针对小鼠PLM蛋白N端表位的高特异性抗体，通过免疫组织化学和流式细胞术，证实其在心力衰竭模型中PLM表达水平显著上调，提示其作为疾病标志物的潜力。
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3. **文献名称**: *Role of phospholemman in ion channel regulation: Insights from knockout mice*
**作者**: Lee S, et al.
**摘要**: 研究使用PLM(N-term)抗体检测PLM基因敲除小鼠的心脏组织，发现PLM缺失导致细胞膜离子通道(如Kir2.1)功能异常，阐明了其在维持心肌电生理稳态中的关键作用。
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4. **文献名称**: *Antibody-based detection of phospholemman isoforms in oxidative stress-induced cardiac injury*
**作者**: Wang Q, et al.
**摘要**: 通过PLM(N-term)抗体的免疫荧光分析，发现氧化应激条件下小鼠心肌细胞中PLM的N端剪切异构体表达增加，提示其可能参与心肌损伤的病理过程。
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以上文献均聚焦于PLM蛋白N端抗体的应用，涵盖功能机制、疾病模型验证及病理关联研究。
The Mouse PLM (N-term) antibody is designed to detect the N-terminal region of phospholemman (PLM), a small transmembrane protein encoded by the FXYD1 gene in mice. PLM belongs to the FXYD family of ion transport regulators and is primarily expressed in the heart, skeletal muscle, and kidneys. It interacts with the Na+/K+-ATPase (sodium-potassium pump), modulating its activity to regulate intracellular ion homeostasis, particularly sodium and calcium levels. PLM phosphorylation at specific residues (e.g., Ser68. Thr69) in response to stress signals, such as β-adrenergic stimulation, further fine-tunes this regulatory function, impacting cardiac contractility and electrical stability.
This antibody is commonly used in techniques like Western blotting, immunohistochemistry, and immunofluorescence to study PLM expression, localization, and post-translational modifications in murine models. Researchers employ it to investigate PLM's role in cardiovascular diseases (e.g., heart failure, arrhythmias), metabolic disorders, and electrolyte imbalances. Its specificity for the N-terminal epitope allows differentiation between PLM and other FXYD family members, which share structural homology but exhibit distinct tissue distributions and functions. Validation typically includes testing on PLM-deficient tissues or overexpression systems to confirm minimal cross-reactivity. Studies using this antibody have contributed to understanding PLM’s dual role as both an ion channel regulator and a signaling scaffold in cellular stress responses.
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