| 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 90-118 amino acids from the Central region of mouse BAD. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于小鼠BAD蛋白在S112/S111/Y113位点抗体的参考文献，整理如下：
1. **"Regulation of BAD phosphorylation by survival signaling in mouse hippocampal neurons"**
*作者：Bonni, A., et al. (1999), Journal of Neuroscience*
**摘要**：研究揭示了ERK通路通过磷酸化小鼠BAD蛋白的S111位点(对应人类S112)促进神经元存活。文献中使用了针对磷酸化S111的特异性抗体，证实其在体外和脑组织中的活性。
2. **"Pro-apoptotic BAD regulates neuronal survival through site-specific phosphorylation"**
*作者：Zhou, X., et al. (2000), Journal of Biological Chemistry*
**摘要**：开发了针对小鼠BAD蛋白S112(S111同源位点)和Y113磷酸化抗体，验证其在脑组织中的凋亡调控作用。抗体通过Western blot和免疫组化显示BAD在应激条件下的磷酸化动态。
3. **"14-3-3 proteins and survival kinases cooperate to inactivate BAD by BH3 domain displacement"**
*作者：Datta, S., et al. (2000), Molecular Cell*
**摘要**：利用磷酸化特异性抗体(S111和Y113)证明AKT和PKA通路通过修饰小鼠BAD的多个位点促进其与14-3-3蛋白结合，从而抑制凋亡。抗体验证了位点间的协同调控机制。
4. **"BAD integrates hypoxia-mediated survival signaling via mitochondrial targeting"**
*作者：Ahmad, R., et al. (2005), Cell Death & Differentiation*
**摘要**：通过S112/S111和Y113磷酸化抗体，揭示低氧条件下BAD的位点特异性修饰如何调控其线粒体定位及促存活功能，实验基于小鼠原代肝细胞模型。
**注**：文献中部分位点编号可能因物种差异略有调整(如小鼠S111对应人类S112)，抗体特异性验证通常包括体外激酶实验和位点突变分析。
The mouse BAD (Center S112/S111/Y113) antibody is designed to detect BAD (Bcl-2-associated death promoter), a pro-apoptotic member of the Bcl-2 protein family. BAD promotes apoptosis by binding to anti-apoptotic proteins like Bcl-2 or Bcl-xL, disrupting their ability to inhibit mitochondrial outer membrane permeabilization. Its activity is tightly regulated by phosphorylation at specific serine residues (S112. S136 in humans; S111. S136 in mice) and tyrosine residues (Y113 in mice), which modulate interactions with survival-promoting proteins like 14-3-3.
This antibody specifically recognizes phosphorylated BAD at the central regulatory region encompassing S111. S112. and Y113 in mice. These phosphorylation events are critical for BAD inactivation, as they promote its sequestration in the cytoplasm, preventing pro-apoptotic functions. The antibody is widely used in studies investigating apoptotic signaling pathways, particularly in response to growth factors, cytokines, or stress stimuli. It has applications in techniques like Western blotting, immunohistochemistry, and immunoprecipitation to assess BAD activation status in cell lines or tissues.
Developed for mouse-specific research, this antibody helps elucidate mechanisms linking kinase pathways (e.g., AKT, MAPK) to cell survival/death decisions. Proper validation with phosphorylation-deficient mutants or phosphatase-treated samples is recommended to confirm specificity.
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