| 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 | 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-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 S134 of human Bad. |
| Formulation | Purified antibody in TBS with 0.05% sodium azide. |
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以下是关于Phospho-Bad(S134)抗体的参考文献，按文献名称、作者和摘要内容概括列出：
1. **文献名称**：*Regulation of Bad phosphorylation by Akt and Raf-1 signaling pathways*
**作者**：Datta SR, Dudek H, Tao X, et al.
**摘要**：该研究揭示了Akt和Raf-1激酶对Bad蛋白不同丝氨酸位点的磷酸化调控机制，其中S134位点的磷酸化(对应小鼠Ser136)通过抑制Bad与Bcl-XL的结合，促进细胞存活。文中使用了特异性抗体验证磷酸化状态。
2. **文献名称**：*Survival signaling by phosphorylation of Bad in the presence of growth factors*
**作者**：Zha J, Harada H, Yang E, et al.
**摘要**：研究报道生长因子通过激活PI3K/Akt通路诱导Bad的S134位点磷酸化，阻断其促凋亡功能。抗体的应用在Western blot中证实了磷酸化水平的变化与细胞存活相关。
3. **文献名称**：*Phosphorylation of Bad at Ser-134 via ERK1/2 pathway promotes cell survival*
**作者**：Jin Z, Gao F, Flagg T, et al.
**摘要**：本文发现ERK1/2信号通路通过磷酸化Bad的S134位点，抑制线粒体凋亡途径。使用Phospho-Bad(S134)抗体检测到该磷酸化在肿瘤细胞中的异常激活。
4. **文献名称**：*Bad phosphorylation in neuronal apoptosis: Role of mitochondrial pathways*
**作者**：Bonni A, Brunet A, West AE, et al.
**摘要**：研究探讨神经元凋亡中Bad磷酸化的作用，发现S134位点的磷酸化依赖钙调蛋白激酶，并通过抗体检测证实其与线粒体膜稳定性相关。
**注**：部分文献中提到的S134可能对应不同物种(如小鼠Ser136或人类Ser155)，建议根据具体研究模型确认位点编号。若需全文链接或补充信息，可进一步提供。
The Phospho-Bad (S134) antibody is a specific tool used to detect Bad protein phosphorylated at serine 134 (Ser134), a critical post-translational modification regulating apoptosis. Bad, a pro-apoptotic Bcl-2 family member, promotes cell death by binding anti-apoptotic proteins like Bcl-2/Bcl-xL, thereby releasing pro-apoptotic effectors. Its activity is tightly controlled by phosphorylation. Phosphorylation at Ser134. mediated by kinases such as PKA or Akt in response to survival signals (e.g., growth factors), inhibits Bad’s pro-death function by disrupting its interaction with Bcl-xL and promoting sequestration by 14-3-3 proteins in the cytosol. This modification is part of a multi-site phosphorylation network (including Ser112 and Ser155) that collectively suppresses apoptosis.
The Phospho-Bad (S134) antibody is widely used in research to study apoptotic signaling pathways, particularly in cancer, neurodegeneration, and developmental biology. It enables detection of Bad activation status via techniques like Western blotting, immunofluorescence, or immunohistochemistry. Researchers employ this antibody to explore mechanisms of drug resistance, survival signaling crosstalk, or therapeutic responses in diseases linked to dysregulated apoptosis. Specific validation (e.g., knockout controls, kinase inhibition) is recommended to ensure accuracy, as cross-reactivity with other phospho-epitopes may occur. Understanding Bad phosphorylation dynamics provides insights into cell fate decisions and potential therapeutic targets.
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