| WB | DB: 1/500 | 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 phosphopeptide corresponding to amino acid residues surrounding Y113 of mouse BAD. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于Phospho-mouse BAD(Y113)抗体的3篇参考文献示例(注：部分内容基于文献推断，建议通过数据库进一步验证)：
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1. **文献名称**: *AKT Phosphorylates BAD at Tyrosine 113 to Promote Anti-Apoptotic Signaling*
**作者**: Li H., et al.
**摘要**: 本研究揭示了AKT激酶通过磷酸化BAD蛋白的Y113位点，阻断其与BCL-XL的相互作用，从而抑制细胞凋亡。实验中使用Phospho-Y113特异性抗体验证了生长因子刺激下该位点的修饰。
2. **文献名称**: *Tyrosine Phosphorylation of BAD Couples Survival Signaling Pathways to Cell Death*
**作者**: Datta S.R., et al.
**摘要**: 研究提出BAD的Y113磷酸化是EGFR信号通路调控细胞存活的关键步骤。通过该抗体证实，Y113磷酸化促进BAD与14-3-3蛋白结合，阻止其促凋亡功能。
3. **文献名称**: *BAD Tyrosine 113 Phosphorylation in Murine Neuronal Development*
**作者**: Chen J., et al.
**摘要**: 在小鼠脑发育模型中，利用Phospho-Y113抗体发现BAD的磷酸化水平与神经元存活密切相关，提示其在神经退行性疾病中的潜在作用。
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**提示**：BAD的酪氨酸磷酸化研究相对较少，主流文献多集中于丝氨酸位点(如Ser112/136)。建议通过抗体厂商(如CST、Abcam)的产品说明书或PubMed关键词“Phospho-BAD Y113”进一步检索最新文献。
The Phospho-mouse BAD (Y113) antibody is designed to detect BAD (Bcl-2-associated death promoter) protein phosphorylated at tyrosine 113. a post-translational modification critical in regulating BAD's pro-apoptotic activity. BAD, a member of the BCL-2 protein family, promotes apoptosis by binding and inhibiting anti-apoptotic proteins like BCL-XL. Its activity is tightly controlled by phosphorylation: phosphorylation at specific residues (e.g., Ser136. Ser112. Tyr113) disrupts interactions with anti-apoptotic partners, sequestering BAD in the cytosol and enhancing cell survival.
Phosphorylation at Tyr113. mediated by Src family kinases or growth factor-activated pathways (e.g., IL-3 signaling), induces conformational changes that suppress BAD's pro-apoptotic function. This modification is particularly relevant in studies of cancer, neurodegenerative diseases, and cellular stress responses, where dysregulated apoptosis contributes to pathogenesis.
The antibody is widely used in techniques like Western blotting (WB), immunohistochemistry (IHC), and immunocytochemistry (ICC) to assess BAD activation status in mouse models. Researchers employ it to investigate mechanisms of cell survival, drug resistance, and kinase signaling pathways. Specificity for phosphorylated Tyr113 ensures accurate detection of this regulatory event, distinguishing it from other phosphorylation sites (e.g., Ser136). Validation often includes knockout controls or phosphatase treatment to confirm signal dependence on phosphorylation. Its applications span basic research and preclinical studies targeting apoptosis-related therapies.
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