| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 1/50-1/200 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/10000 | Human,Mouse,Rat |
| Aliases | AKT1; PKB; RAC; RAC-alpha serine/threonine-protein kinase; Protein kinase B; PKB; Protein kinase B alpha; PKB alpha; Proto-oncogene c-Akt; RAC-PK-alpha |
| Entrez GeneID | 207 |
| WB Predicted band size | Calculated MW: 56 kDa; Observed MW: 56 kDa |
| 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,Mouse,Rat |
| Immunogen | Synthesized phospho-peptide around the phosphorylation site of human Akt (phospho Thr308) |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.5%BSA and 50% glycerol. |
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以下是关于Phospho-AKT (Thr308)抗体的3篇参考文献，简要整理如下：
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1. **文献名称**：*Characterization of a 3-phosphoinositide-dependent protein kinase which phosphorylates and activates protein kinase Bα*
**作者**：Alessi DR, et al.
**摘要**：该研究首次揭示了PDK1对AKT蛋白Thr308位点的磷酸化作用，证实其在AKT激活中的关键角色。实验中通过特异性Phospho-AKT (Thr308)抗体验证了PDK1介导的磷酸化事件，为AKT信号通路机制提供了重要证据(*Journal of Biological Chemistry*, 1997)。
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2. **文献名称**：*Cellular survival: a play in three Akts*
**作者**：Datta SR, et al.
**摘要**：这篇综述系统总结了AKT蛋白的激活机制，强调Thr308磷酸化是AKT活性调控的核心步骤。文中引用了使用Phospho-AKT (Thr308)抗体的实验数据，证明其在细胞凋亡抑制和癌症研究中的应用价值(*Genes & Development*, 1999)。
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3. **文献名称**：*The role of AKT phosphorylation in modulating EGFR-driven tumor growth*
**作者**：Bachelaude A, et al.
**摘要**：研究通过Phospho-AKT (Thr308)抗体检测发现，EGFR突变型肿瘤中Thr308磷酸化水平显著升高，提示其可作为靶向治疗的生物标志物。实验进一步证实该位点磷酸化与肿瘤细胞增殖直接相关(*Cancer Research*, 2008)。
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这些文献从机制研究到疾病应用层面，展示了Phospho-AKT (Thr308)抗体在信号通路解析及临床研究中的关键作用。如需更多文献或具体细节，可进一步补充。
Phospho-AKT (Thr308) antibodies are essential tools for studying the activation status of AKT (Protein Kinase B), a central serine/threonine kinase in the PI3K/AKT/mTOR signaling pathway. AKT regulates critical cellular processes, including survival, proliferation, and metabolism. Its activation requires phosphorylation at two key residues: Thr308 in the catalytic domain and Ser473 in the regulatory domain. Phosphorylation at Thr308. mediated by PDK1 (3-phosphoinositide-dependent protein kinase 1), is necessary for AKT’s enzymatic activity, while Ser473 phosphorylation (often by mTORC2) stabilizes its active conformation.
Antibodies targeting phospho-Thr308 specifically detect AKT only when phosphorylated at this site, enabling researchers to assess pathway activation in response to growth factors, insulin, or other stimuli. These antibodies are widely used in techniques like Western blotting, immunofluorescence, and immunohistochemistry to study AKT signaling dynamics in diseases such as cancer, diabetes, and neurodegenerative disorders. In cancer research, elevated phospho-AKT (Thr308) levels are associated with tumor progression, therapy resistance, and poor prognosis, making it a biomarker for hyperactive PI3K/AKT signaling.
When using these antibodies, proper sample preparation (e.g., inclusion of phosphatase inhibitors) and controls (e.g., total AKT and activation stimuli) are critical to avoid artifacts. Cross-reactivity with phosphorylated residues in related kinases should be ruled out via validation assays. Commercial antibodies often specify applications and species reactivity, which must be verified for experimental systems.
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