| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | 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 | CDC25M2; MPIP2; Dual specificity phosphatase Cdc25B; CDC25HU2; |
| Entrez GeneID | 994; |
| WB Predicted band size | 64kDa |
| 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 |
| Immunogen | Peptide sequence around phosphorylation site of serine 353(R-R-S(p)-V-T) derived from Human CDC25B . |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
+ +
以下是关于CDC25B (Phospho-Ser353)抗体的示例参考文献(注：以下内容为示例，实际文献需通过学术数据库检索)：
---
1. **"CDC25B phosphorylation at Ser353 regulates mitotic entry and DNA damage response"**
*Author: Lee et al. (2018)*
**摘要**: 研究揭示了CDC25B在Ser353位点的磷酸化通过抑制其磷酸酶活性调控G2/M期转换，使用Phospho-Ser353特异性抗体证实该修饰在DNA损伤后由CHK1激酶介导，导致细胞周期阻滞。
2. **"Phosphorylation-dependent subcellular localization of CDC25B in ovarian cancer cells"**
*Author: Zhang et al. (2020)*
**摘要**: 通过Phospho-Ser353抗体分析发现，Ser353磷酸化促进CDC25B在细胞质滞留，抑制其进入细胞核启动有丝分裂，该机制与卵巢癌化疗耐药性相关。
3. **"A novel role of CDC25B-Ser353 phosphorylation in regulating centrosome amplification"**
*Author: Gupta et al. (2019)*
**摘要**: 研究利用Phospho-Ser353抗体证明，该位点的磷酸化异常导致中心体过度复制，促进基因组不稳定性，为癌症靶向治疗提供潜在靶点。
4. **"Development of a phospho-specific antibody for CDC25B Ser353 and its application in hepatocellular carcinoma"**
*Author: Wang et al. (2021)*
**摘要**: 报道了一种高特异性Phospho-Ser353抗体的开发，并应用于肝癌样本检测，发现该位点磷酸化水平与肿瘤分级和预后不良显著相关。
---
**建议**：实际文献可通过PubMed、Google Scholar等平台以关键词“CDC25B Phospho-Ser353 antibody”“CDC25B Ser353 phosphorylation”检索，重点关注抗体验证方法(如Western blot、免疫组化)及功能研究部分。
The CDC25B (Phospho-Ser353) antibody is a specialized tool used to study the phosphorylation status of CDC25B, a dual-specificity phosphatase critical for cell cycle regulation. CDC25B belongs to the CDC25 family, which activates cyclin-dependent kinases (CDKs) by removing inhibitory phosphorylation marks, thereby driving cell cycle progression. Specifically, CDC25B facilitates the G2/M transition by dephosphorylating CDK1 at Tyr15. Phosphorylation at Ser353 (and other residues) is a key regulatory mechanism controlling CDC25B activity, stability, and subcellular localization.
This phosphorylation event is often induced by DNA damage or replication stress, triggering checkpoint responses. For example, kinases like CHK1/CHK2 phosphorylate CDC25B at Ser353 in response to DNA damage, leading to its cytoplasmic sequestration or proteasomal degradation. This prevents premature entry into mitosis, allowing time for DNA repair. The CDC25B (Phospho-Ser353) antibody specifically detects this post-translational modification, enabling researchers to study cell cycle checkpoint mechanisms, DNA damage responses, and CDC25B's role in cancer. Overexpression or dysregulation of CDC25B is linked to genomic instability and tumorigenesis, making this antibody valuable in cancer research. It is commonly used in techniques like Western blotting, immunofluorescence, and immunohistochemistry to assess phosphorylation dynamics in experimental models or clinical samples. Its applications extend to exploring therapeutic strategies targeting cell cycle regulators in oncology.
×
