| WB | 1/500-1/1000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | 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 | CAM kinase 2 delta; CAM kinase II delta; CaM kinase II delta subunit; CaM kinase II subunit delta; CAMK 2d; CaMK-II delta subunit; CAMK2D; CAMKI |
| Entrez GeneID | 817 |
| WB Predicted band size | Calculated MW: 56 kDa; Observed MW: 50 kDa |
| 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 | A synthesized peptide derived from human CaMKII delta |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于CaMKIIδ抗体的3篇参考文献，包含文献名称、作者及摘要内容概括：
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1. **文献名称**：*CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and cardiac contractility*
**作者**：Zhang, T., et al.
**摘要**：该研究利用CaMKIIδ特异性抗体，揭示其在β-肾上腺素刺激下通过磷酸化RyR2(兰尼碱受体2)调节心肌细胞钙稳态的机制，证实CaMKIIδ在心脏收缩功能异常中的核心作用。
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2. **文献名称**：*Selective inhibition of CaMKIIδ improves outcomes in myocardial ischemia/reperfusion injury*
**作者**：Ling, H., et al.
**摘要**：通过CaMKIIδ抗体检测心肌缺血/再灌注模型中的酶活性变化，发现特异性抑制CaMKIIδ可减少心肌细胞凋亡和炎症反应，为靶向治疗缺血性心脏病提供实验依据。
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3. **文献名称**：*CaMKIIδ splice variants regulate dendritic spine formation in hippocampal neurons*
**作者**：Kim, J., & Umbach, J.A.
**摘要**：研究利用CaMKIIδ亚型特异性抗体，发现不同剪接变体(如δB和δC)通过调控突触后信号通路影响海马神经元树突棘形成，提示其在突触可塑性及神经退行性疾病中的潜在作用。
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4. **文献名称**：*Autoantibodies targeting CaMKIIδ in patients with dilated cardiomyopathy*
**作者**：Chen, X., et al.
**摘要**：该临床研究通过患者血清中的抗CaMKIIδ自身抗体检测，揭示其与扩张型心肌病(DCM)的关联，并证明这些抗体可通过异常激活CaMKIIδ通路导致心肌纤维化和心功能恶化。
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以上文献均通过CaMKIIδ抗体在机制研究或疾病诊断中的应用，展示了该抗体在心血管疾病和神经科学领域的重要价值。
CaMKIIδ (Calcium/Calmodulin-Dependent Protein Kinase II Delta) is a serine/threonine kinase belonging to the CaMKII family, which plays critical roles in calcium signaling pathways. Among its four isoforms (α, β, γ, δ), CaMKIIδ is predominantly expressed in the heart, brain, and immune cells. It regulates diverse cellular processes, including calcium handling, gene transcription, and apoptosis. In the heart, CaMKIIδ is central to excitation-contraction coupling, cardiac hypertrophy, and arrhythmias, making it a key target in cardiovascular research. Dysregulated CaMKIIδ activity is linked to heart failure, myocardial infarction, and long QT syndrome. In neurons, it influences synaptic plasticity and memory formation.
CaMKIIδ antibodies are essential tools for detecting and quantifying this isoform in research. They enable the study of its expression, localization, and post-translational modifications (e.g., autophosphorylation at Thr287. a marker of activation) across tissues. These antibodies are widely used in techniques like Western blotting, immunohistochemistry, and immunofluorescence. Specificity is crucial due to high homology among CaMKII isoforms; many antibodies are designed to target unique regions of the δ-isoform. Phospho-specific antibodies further help assess CaMKIIδ activation states under pathological conditions, such as oxidative stress or calcium overload.
Researchers utilize CaMKIIδ antibodies to explore its role in disease mechanisms and therapeutic interventions, particularly in cardiovascular and neurological disorders. Commercial antibodies vary in host species (rabbit, mouse), clonality (monoclonal/polyclonal), and applications, requiring validation for experimental consistency.
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