| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 1/20 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 1/50-1/200 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | EIF2AK2; PKR; PRKR; Interferon-induced; double-stranded RNA-activated protein kinase; Eukaryotic translation initiation factor 2-alpha kinase 2; eIF-2A protein kinase 2; Interferon-inducible RNA-dependent protein kinase; P1/eIF-2A protein k |
| Entrez GeneID | 5610 |
| WB Predicted band size | Calculated MW: 62 kDa; Observed MW: 74 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 |
| Immunogen | A synthetic peptide of human PKR |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是关于PKR抗体的3篇参考文献及其摘要概括：
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1. **文献名称**：*The Role of Double-Stranded RNA-Dependent Protein Kinase in Interferon-Mediated Antiviral Responses*
**作者**：Williams, B.R.G. et al.
**摘要**：该研究阐明了PKR在干扰素介导的抗病毒免疫中的核心作用，揭示其通过磷酸化eIF2α阻断病毒蛋白合成，并验证了特异性抗体在检测PKR激活状态中的应用。
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2. **文献名称**：*Structural Insights into PKR Activation by dsRNA and ATP Binding*
**作者**：Dar, A.C. & Sicheri, F.
**摘要**：通过X射线晶体学解析了PKR与dsRNA及ATP结合的分子结构，解释了其自抑制状态的解除机制，研究中利用单克隆抗体定位关键功能域以验证构象变化。
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3. **文献名称**：*PKR-Dependent Neuroinflammation in Alzheimer’s Disease Models*
**作者**：Chang, R.C. et al.
**摘要**：发现阿尔茨海默病模型中PKR的异常激活促进神经炎症和tau蛋白过度磷酸化，使用PKR抗体阻断实验证实其病理关联，提示PKR作为潜在治疗靶点。
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**可选补充文献**：
4. **文献名称**：*Targeting PKR with Small Molecule Inhibitors Suppresses Hepatitis C Virus Replication*
**作者**：Garcia, M.A. et al.
**摘要**：证明抑制PKR活性可显著降低HCV复制效率，研究通过抗体检测PKR磷酸化水平验证抑制剂效果，为抗病毒药物开发提供依据。
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以上文献覆盖PKR的分子机制、结构解析及疾病关联研究，均涉及抗体在实验中的关键应用(检测表达、活性或干预验证)。建议结合具体研究方向选择近年高引用论文。
Protein kinase R (PKR), also known as double-stranded RNA (dsRNA)-activated protein kinase, is a key enzyme in innate immunity and cellular stress responses. It is activated by viral dsRNA during infections, triggering phosphorylation of eukaryotic initiation factor 2α (eIF2α) to inhibit viral protein synthesis. PKR also regulates signaling pathways involving NF-κB and MAPK, influencing apoptosis, inflammation, and antiviral defense.
PKR antibodies are essential tools for studying its expression, activation, and interactions in research. They detect PKR in immunoassays (e.g., Western blot, ELISA, immunofluorescence) and help elucidate its role in diseases, including viral infections (e.g., hepatitis C, HIV), neurodegenerative disorders (e.g., Alzheimer’s), and cancer. Phospho-specific antibodies targeting activated PKR (phosphorylated at Thr451/Thr446) are critical for assessing its functional state.
Dysregulation of PKR is linked to chronic inflammation, tumor progression, and autoimmune conditions, making its antibodies valuable for therapeutic research. However, variability in antibody specificity and cross-reactivity requires careful validation in experimental models. Overall, PKR antibodies advance understanding of cellular stress mechanisms and antiviral therapies.
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