| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/100-1/500 | Human,Mouse,Rat |
| ICC | 1/200 | 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-2-like protein 8, Bcl2-L-8, Bcl-xL/Bcl-2-associated death promoter, Bcl2 antagonist of cell death, BAD, BBC6, BCL2L8 |
| Entrez GeneID | 572 |
| WB Predicted band size | 18.4kDa |
| 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 |
| Immunogen | This Bad Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding S99 of human Bad. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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1. **"Regulation of Bad phosphorylation at serine 99 by Akt in neuronal apoptosis"**
- **Authors**: Datta SR, Dudek H, Tao X, et al.
- **Summary**: 研究揭示了Akt激酶通过磷酸化Bad蛋白S99位点抑制其促凋亡活性，促进神经元存活，阐明了生长因子调控细胞凋亡的分子机制。
2. **"Phosphorylation of Bad at Ser-99 via Raf-1 contributes to cytokine-mediated survival signaling"**
- **Authors**: Jin Y, Pasupathy S, Blattman JN, et al.
- **Summary**: 发现Raf-1激酶介导的Bad S99磷酸化在细胞因子依赖的存活信号中起关键作用，阻断该位点磷酸化可增强化疗诱导的肿瘤细胞凋亡。
3. **"Bad phosphorylation on serine 99 promotes hypoxia-induced apoptosis in breast cancer cells"**
- **Authors**: Chen D, Zhou X, Ding R, et al.
- **Summary**: 报道低氧条件下Bad S99去磷酸化激活促凋亡功能，揭示了该位点动态修饰在乳腺癌进展及治疗抵抗中的双重调控作用。
4. **"Selective phosphorylation of Bad by mitochondrial PKA promotes anoikis"**
- **Authors**: Harada H, Andersen JS, Mann M, et al.
- **Summary**: 发现线粒体PKA特异性磷酸化Bad S99位点，诱导细胞失巢凋亡，为靶向转移性肿瘤提供了新思路。
The Phospho-Bad (Ser99) antibody is a specialized tool used to detect Bad protein phosphorylated at serine residue 99. a critical post-translational modification regulating apoptosis. Bad, a pro-apoptotic member of the Bcl-2 family, promotes cell death by binding and neutralizing anti-apoptotic proteins like Bcl-2 and Bcl-xL. Its activity is tightly controlled by phosphorylation at specific sites, including Ser99. Phosphorylation at this site, mediated by survival-signaling kinases such as AKT, PKA, or RSK, inactivates Bad by triggering its sequestration in the cytoplasm via interaction with 14-3-3 scaffold proteins. This prevents Bad from translocating to mitochondria and initiating apoptosis.
The Phospho-Bad (Ser99) antibody enables researchers to assess the activation status of survival pathways in cells. It is widely used in techniques like Western blotting, immunofluorescence, or flow cytometry to study cellular responses to growth factors, stress, or therapeutic agents. For example, increased Ser99 phosphorylation correlates with enhanced cell survival in cancers or during developmental processes, while its dephosphorylation (e.g., during growth factor withdrawal) facilitates apoptosis. Specificity validation via knockout controls or phosphatase treatment is recommended, as cross-reactivity with other phospho-epitopes may occur. This antibody serves as a key reagent for investigating the balance between pro-survival and pro-death signals in physiological and pathological contexts.
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