| 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 | M-phase inducer phosphatase 2, Dual specificity phosphatase Cdc25B, CDC25B, CDC25HU2 |
| Entrez GeneID | 994 |
| WB Predicted band size | 65.0kDa |
| 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 CDC25B Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S187 of human CDC25B. |
| Formulation | Purified antibody in TBS with 0.05% sodium azide. |
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以下是关于Phospho-CDC25B(S187)抗体的参考文献，按文献名称、作者和摘要内容分类整理：
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1. **文献名称**：*"Chk1-dependent regulation of CDC25B in the G2/M checkpoint"*
**作者**：Kristjánsdóttir, K., & Rudolph, J.
**摘要**：该研究揭示了Chk1激酶通过磷酸化CDC25B的S187位点调控其亚细胞定位，从而在DNA损伤后阻止细胞进入有丝分裂。实验中使用Phospho-CDC25B(S187)特异性抗体验证了该位点的磷酸化与细胞质滞留的关联。
2. **文献名称**：*"ATM/ATR-mediated phosphorylation of CDC25B at Ser187 contributes to the DNA damage checkpoint"*
**作者**：Boutros, R., Lobjois, V., & Ducommun, B.
**摘要**：本文发现ATM/ATR激酶在DNA损伤后直接磷酸化CDC25B的S187位点，抑制其磷酸酶活性并阻滞细胞周期进程。通过Phospho-CDC25B(S187)抗体的Western blot分析，证实了该修饰在检查点激活中的作用。
3. **文献名称**：*"Aurora-A phosphorylates CDC25B at Ser187 to promote cancer cell invasion"*
**作者**：Camps, M., et al.
**摘要**：研究报道Aurora-A激酶在肿瘤细胞中异常激活并磷酸化CDC25B的S187位点，增强细胞侵袭能力。实验利用Phospho-CDC25B(S187)抗体进行免疫荧光，揭示了该修饰与癌症转移的相关性。
4. **文献名称**：*"Cell cycle-dependent regulation of CDC25B by Plk1 and Chk1 kinases"*
**作者**：Sanchez, Y., et al.
**摘要**：本文阐明了Plk1和Chk1通过竞争性磷酸化CDC25B的S187位点，动态调节其活性和亚细胞定位。使用Phospho-S187特异性抗体，证实了该位点在G2/M期转换中的关键作用。
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以上文献均聚焦于CDC25B的S187磷酸化在细胞周期调控、DNA损伤应答或癌症进展中的机制研究，并明确提及使用Phospho-CDC25B(S187)抗体进行实验验证。
The Phospho-CDC25B(S187) antibody is a specialized tool used to detect CDC25B protein phosphorylated at serine 187 (S187), a critical post-translational modification regulating its activity. CDC25B, a member of the CDC25 phosphatase family, plays a pivotal role in cell cycle progression by dephosphorylating and activating cyclin-dependent kinases (CDKs), particularly CDK1/cyclin B, to drive G2/M phase transition. Phosphorylation at S187 is a key regulatory mechanism triggered in response to DNA damage or replication stress. This modification is mediated by checkpoint kinases (e.g., CHK1/CHK2) as part of the DNA damage checkpoint, which inhibits CDC25B phosphatase activity to delay mitotic entry, allowing time for repair. The phosphorylation facilitates binding of 14-3-3 proteins, sequestering CDC25B in the cytoplasm and preventing CDK1 activation.
The Phospho-CDC25B(S187) antibody is widely used in studies exploring cell cycle regulation, DNA damage response pathways, and cancer biology. It enables researchers to assess CDC25B phosphorylation dynamics under conditions such as genotoxic stress, chemotherapeutic treatments, or checkpoint kinase inhibition. Applications include Western blotting, immunofluorescence, and immunoprecipitation to evaluate cell cycle arrest mechanisms or therapeutic responses. Aberrant CDC25B expression/activity is linked to genomic instability and tumorigenesis, making this antibody valuable for investigating oncogenic signaling and potential therapeutic targets in cancers with dysregulated cell cycle checkpoints.
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