| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/100-1/500 | 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 | Serine/threonine-protein kinase PLK2, Polo-like kinase 2, PLK-2, hPlk2, Serine/threonine-protein kinase SNK, hSNK, Serum-inducible kinase, PLK2, SNK |
| Entrez GeneID | 10769 |
| WB Predicted band size | 78.2kDa |
| 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 PLK2 (SNK) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 375-406 amino acids from the C-terminal region of human PLK2 (SNK). |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,1%BSA and 50% glycerol.prepared by Saturated Ammonium Sulfate (SAS) . |
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以下是关于PLK2(SNK)抗体的3篇参考文献摘要示例(文献名称及内容为虚拟简化版，供参考)：
1. **文献名称**: *"PLK2 regulates synaptic plasticity and Alzheimer's disease-associated neuronal loss"*
**作者**: Kaushik et al. (2015)
**摘要**: 使用PLK2特异性抗体研究发现，PLK2在小鼠海马神经元中响应活性依赖性信号上调，促进突触修剪和Aβ蛋白毒性环境下的神经元凋亡，提示其在阿尔茨海默病病理中的作用。
2. **文献名称**: *"PLK2 acts as a tumor suppressor in breast cancer by modulating cell cycle progression"*
**作者**: Li et al. (2018)
**摘要**: 通过PLK2抗体免疫组化分析，发现乳腺癌组织中PLK2表达显著下调，且其低表达与患者预后不良相关。体外实验证实PLK2过表达通过阻滞G1/S期抑制肿瘤增殖。
3. **文献名称**: *"SNK/PLK2 inhibition promotes neuroblastoma differentiation via MYCN downregulation"*
**作者**: Burns et al. (2020)
**摘要**: 研究使用PLK2抗体检测神经母细胞瘤模型中的蛋白表达，发现抑制PLK2活性可降低MYCN致癌基因稳定性，诱导肿瘤细胞分化，为靶向治疗提供新策略。
4. **文献名称**: *"PLK2 phosphorylates CDC25C to mediate cell cycle checkpoint recovery after DNA damage"*
**作者**: Mochida et al. (2016)
**摘要**: 利用PLK2特异性抗体进行免疫印迹分析，揭示PLK2在DNA损伤修复后通过磷酸化CDC25C调控G2/M期检查点恢复，确保基因组稳定性。
(注：以上文献名为虚构示例，实际文献需通过PubMed/Google Scholar检索确认。)
The Polo-like kinase 2 (PLK2), also known as serum-inducible kinase (SNK), is a serine/threonine kinase belonging to the Polo-like kinase family. Primarily expressed in the brain and testes, PLK2 plays critical roles in cell cycle regulation, synaptic plasticity, and neuronal homeostasis. It is activated during the G1/S phase and post-mitotic phases, where it regulates centrosome maturation, mitotic entry, and DNA damage response. In neurons, PLK2 is involved in activity-dependent structural remodeling, including dendritic spine formation and elimination, by modulating pathways like the ubiquitin-proteasome system and autophagy.
PLK2 antibodies are widely used in research to detect protein expression, localization, and phosphorylation status in various models, including cancer and neurological disorders. These antibodies are essential tools for Western blotting, immunohistochemistry, and immunofluorescence. PLK2 dysregulation has been implicated in diseases such as Alzheimer's, Parkinson's, and cancers. For instance, PLK2 overexpression may suppress tumor growth in certain contexts, while its deficiency is linked to synaptic dysfunction in neurodegenerative conditions. However, some studies suggest conflicting roles (e.g., pro-survival vs. pro-apoptotic effects), highlighting context-dependent functions.
Researchers must validate PLK2 antibodies for specificity, as cross-reactivity with other PLK family members (e.g., PLK1/PLK3) is common. Epitope mapping and knockout controls are recommended. Commercial antibodies often target regions like the catalytic kinase domain or C-terminal polo-box domain. Understanding PLK2's dual roles in health and disease continues to drive interest in therapeutic targeting, with antibodies aiding mechanistic studies and biomarker discovery.
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