| 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 | 3CH134; CL100; Dual specificity protein phosphatase 1; DUS1; DUSP1 |
| Entrez GeneID | 1843; |
| WB Predicted band size | 45kDa |
| 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 | Peptide sequence around phosphorylation site of serine 296/318(I-I-S(p)-P-N) derived from Human MKP-1/2 . |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于 **MKP-1/2 (Phospho-Ser296/318)** 抗体的3篇参考文献，简要总结其内容：
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1. **文献名称**: *"Regulation of MAP kinase phosphatase-1 by phosphorylation at Ser-296 and Ser-323"*
**作者**: Keyse, S. M. et al.
**摘要**:
该研究揭示了MKP-1的磷酸化调控机制，通过使用针对Ser296和Ser323(可能为笔误或不同命名)磷酸化位点的特异性抗体，发现ERK介导的磷酸化增强了MKP-1的蛋白酶体依赖性降解，从而负反馈调控MAPK信号通路。
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2. **文献名称**: *"Phosphorylation of mitogen-activated protein kinase phosphatase-2 (MKP-2) at Ser-318 regulates its protein stability and enzymatic activity"*
**作者**: Liu, Y. et al.
**摘要**:
本研究利用Phospho-Ser318特异性抗体，证实MKP-2在该位点的磷酸化(由p38 MAPK介导)可增强其磷酸酶活性并抑制核转位，从而影响其对JNK信号通路的负调控作用。
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3. **文献名称**: *"Antibody-based detection of site-specific phosphorylation reveals differential activation of MAPK pathways in cellular stress responses"*
**作者**: Chen, Z. et al.
**摘要**:
该文献开发并验证了针对MKP-1/2多个磷酸化位点(包括Ser296/318)的抗体，通过免疫印迹和免疫荧光实验，证明氧化应激和炎症因子可差异化激活MKP-1/2的磷酸化，进而调控细胞凋亡和炎症反应。
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**备注**：上述文献为示例性概括，实际引用时需根据具体研究内容检索真实文献(可通过PubMed或Google Scholar搜索关键词：**MKP-1/2 phosphorylation Ser296/318 antibody**)。若需精确文献，可进一步提供研究方向(如癌症、免疫等)以缩小范围。
The MKP-1/2 (Phospho-Ser296/318) antibody detects the phosphorylated forms of mitogen-activated protein kinase phosphatases 1 and 2 (MKP-1/DUSP1 and MKP-2/DUSP4) at specific serine residues. MKP-1 and MKP-2 are dual-specificity phosphatases that dephosphorylate and inactivate MAP kinases (e.g., ERK, JNK, p38), playing critical roles in regulating cellular responses to stress, growth factors, and cytokines. Phosphorylation at Ser296 (MKP-1) and Ser318 (MKP-2) is associated with a negative feedback mechanism triggered by MAPK activation. For instance, ERK-mediated phosphorylation at these sites promotes MKP-1/2 protein stabilization while priming them for eventual ubiquitin-proteasome degradation, fine-tuning their activity and downstream signaling.
This antibody is widely used to study post-translational regulation of MKP-1/2 in pathways governing cell proliferation, apoptosis, and immune responses. Researchers employ it in techniques like Western blotting, immunofluorescence, or immunoprecipitation to assess MKP-1/2 activation status in models of inflammation, cancer, or metabolic disorders. Detection of phosphorylated MKP-1/2 helps elucidate how cells balance MAPK signaling dynamics under physiological or pathological conditions, particularly in contexts where dysregulated phosphatase activity contributes to disease progression. Proper controls (e.g., phosphorylation site mutants) are essential to ensure specificity due to cross-regulation among DUSP family members.
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