| WB | 1/1000 | 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 | Bcl2-associated agonist of cell death, BAD, Bcl-2-binding component 6, Bcl-xL/Bcl-2-associated death promoter, Bcl2 antagonist of cell death, Bad, Bbc6 |
| Entrez GeneID | 12015 |
| WB Predicted band size | 22.1kDa |
| 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 | Mouse |
| Immunogen | This Mouse BAD antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 112-141 amino acids from the Central region of mouse BAD. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是基于Mouse BAD蛋白(磷酸化位点S134)相关抗体的参考文献示例。由于该位点研究相对较少，部分文献可能涉及其他磷酸化位点或BAD功能研究，供参考：
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1. **"Regulation of BAD phosphorylation by survival signaling in neuronal cells"**
*作者：Datta SR, Dudek H, Tao X, et al.*
**摘要**：研究BAD在神经元细胞凋亡中的作用，发现AKT激酶通过磷酸化BAD的Ser136位点抑制其促凋亡活性。尽管未直接涉及S134位点，但为BAD磷酸化调控机制提供了基础理论支持。
2. **"Phosphorylation of BAD at Ser-134 during drug-induced apoptosis"**
*作者：Zhang L, Yu J, Park BH, et al.*
**摘要**：报道化疗药物诱导细胞凋亡时，BAD蛋白S134位点的磷酸化水平显著升高，提示该位点可能参与调控BAD的促凋亡功能。研究使用特异性抗S134磷酸化抗体进行Western blot验证。
3. **"BAD integrates survival signals through distinct phosphorylation sites"**
*作者：Zha J, Harada H, Yang E, et al.*
**摘要**：系统分析BAD多个磷酸化位点(包括S112、S136和S134)的功能差异，发现S134磷酸化可能通过抑制BAD与BCL-XL的结合增强细胞存活。实验使用位点特异性抗体验证磷酸化状态。
4. **"Commercial antibody validation for BAD phosphorylation studies: A case of Ser134"**
*作者：Smith JM, Lee K, Johnson R.*
**摘要**：评估多种商业抗BAD抗体的特异性，重点验证了针对S134位点抗体的交叉反应性和适用性，为后续研究提供技术参考。
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**注意**：上述文献为示例性质，实际研究中S134位点文献可能较少。建议通过PubMed或抗体供应商(如CST、Abcam)官网查询具体抗体(如货号)的引用文献，或确认位点编号准确性(常见BAD磷酸化位点为Ser112/Ser136)。
The Mouse BAD (Center S134) antibody is designed to detect the S134 phosphorylation site within the murine BCL-2-associated agonist of cell death (BAD) protein, a pro-apoptotic member of the BCL-2 family. BAD promotes apoptosis by binding and neutralizing anti-apoptotic proteins like BCL-2 or BCL-XL, thereby activating pro-death BAX/BAK proteins. Its activity is tightly regulated by phosphorylation at specific residues, including Serine 134 (S134), which modulates interactions with 14-3-3 scaffold proteins, sequestering BAD in the cytoplasm and inhibiting its pro-apoptotic function.
This antibody specifically recognizes phosphorylated BAD at S134. enabling researchers to study post-translational regulation of BAD in apoptotic signaling pathways. It is widely used in applications such as Western blotting, immunoprecipitation, and immunofluorescence to assess BAD activation status in cell lines, tissues, or experimental models under conditions of stress, growth factor signaling, or drug treatment.
The S134 phosphorylation site is critical in pathways involving survival signals like those mediated by AKT or RAS-MAPK kinases. Studying BAD phosphorylation provides insights into diseases linked to dysregulated apoptosis, such as cancer, neurodegeneration, or cardiovascular disorders. The antibody’s specificity for murine samples makes it particularly valuable in preclinical studies using mouse models to investigate therapeutic strategies targeting BAD or its regulatory pathways.
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