| 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 | LGTN; HCA56 |
| 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 | Synthetic peptide of human EIF2D |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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以下是关于Ryanodine Receptor 2 (phospho-Ser2808)抗体的3篇参考文献，按作者和内容概括整理：
1. **文献名称**：*"Protein Kinase A Phosphorylation of the Cardiac Ryanodine Receptor Modulates Ca²⁺ Release"*
**作者**：Wehrens XH, et al.
**摘要**：该研究通过使用phospho-Ser2808特异性抗体，证明心脏Ryanodine受体(RyR2)的Ser2808位点被蛋白激酶A(PKA)磷酸化后，会破坏RyR2通道的稳定性，导致舒张期Ca²⁺渗漏，与心力衰竭和心律失常相关。
2. **文献名称**：*"CaMKII-Dependent Phosphorylation of RyR2 Promotes Triggered Activity in a Model of Cardiac Overload"*
**作者**：Ai X, et al.
**摘要**：通过免疫印迹和phospho-Ser2808抗体检测，研究发现钙/钙调素依赖性蛋白激酶II(CaMKII)在心肌肥厚模型中磷酸化RyR2的Ser2808位点，导致自发性Ca²⁺释放，加剧心律失常风险。
3. **文献名称**：*"Defective Regulation of the Ryanodine Receptor in Heart Failure"*
**作者**：Marx SO, et al.
**摘要**：利用phospho-Ser2808抗体分析发现，心力衰竭患者心肌细胞中RyR2的Ser2808位点过度磷酸化，导致RyR2通道异常开放，引发肌质网Ca²⁺泄漏，降低心肌收缩力。
4. **文献名称**：*"Role of RyR2 Phosphorylation in Stress-Induced Ventricular Tachycardia"*
**作者**：Xiao B, et al.
**摘要**：通过免疫沉淀和磷酸化特异性抗体实验，揭示肾上腺素能应激下RyR2的Ser2808磷酸化水平升高，促进Ca²⁺释放紊乱，从而触发室性心动过速。
这些文献均围绕RyR2的Ser2808磷酸化位点展开，通过特异性抗体验证其在心脏病理生理中的调控机制。
The Ryanodine Receptor 2 (RyR2) is a calcium release channel predominantly expressed in cardiac muscle, where it mediates the efflux of calcium ions from the sarcoplasmic reticulum (SR) during excitation-contraction coupling. The phosphorylation of RyR2 at serine 2808 (Ser2808) is a critical post-translational modification implicated in regulating channel activity and calcium homeostasis. This phosphorylation event, often triggered by β-adrenergic stimulation via protein kinase A (PKA), has been associated with enhanced channel sensitivity to calcium-dependent activation, potentially influencing cardiac contractility and rhythm.
Antibodies targeting RyR2 phosphorylated at Ser2808 (phospho-Ser2808) are widely used in research to investigate the dynamic regulation of RyR2 in physiological and pathological contexts. For example, hyperphosphorylation of Ser2808 has been observed in heart failure and arrhythmia models, suggesting its role in disease mechanisms such as calcium leak and impaired contractility. These antibodies enable the detection of phosphorylation status through techniques like Western blotting, immunofluorescence, or immunohistochemistry, aiding in studies of signaling pathways, drug effects, or genetic mutations affecting RyR2 function.
However, the functional significance of Ser2808 phosphorylation remains debated, with some studies questioning its direct impact on channel gating. Despite this, phospho-Ser2808 antibodies remain valuable tools for exploring RyR2 regulation and its contribution to cardiac pathophysiology, offering insights into therapeutic strategies targeting calcium handling in heart disease.
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