| WB | 咨询技术 | 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 | FOXO3, AF6q21, AF6q21 protein, Forkhead box O3, Forkhead box O3A, FOXO3A, FKHRL1P2, Forkhead box protein O3, FOXO2, FKHRL1 |
| Entrez GeneID | 2309; |
| WB Predicted band size | 97kDa |
| 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 | A synthesized peptide derived from human FKHRL1 (Phospho-Ser315) |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 30% glycerol. |
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以下是关于FKHRL1 (Phospho-Ser315)抗体的3篇参考文献及其摘要概括：
1. **文献名称**：*"Regulation of the Forkhead Transcription Factor FKHRL1 by AKT and Stress-Activated Protein Kinase/p38"*
**作者**：Brunet, A. et al.
**摘要**：该研究揭示了AKT和p38激酶对FKHRL1(FOXO3a)磷酸化的调控机制，其中Ser315位点的磷酸化参与调控细胞凋亡和氧化应激响应。实验中使用Phospho-Ser315抗体验证了该位点的修饰对核-质转位的影响。
2. **文献名称**：*"Phosphorylation of FKHRL1 on Serine 315 Promotes Interaction with 14-3-3 Proteins and Cytoplasmic Localization"*
**作者**：Huang, H. et al.
**摘要**：文章阐明了FKHRL1 Ser315磷酸化通过促进与14-3-3蛋白的结合，抑制其转录活性并促进胞质滞留。研究利用特异性Phospho-Ser315抗体，通过免疫印迹和免疫荧光证实了磷酸化依赖性定位变化。
3. **文献名称**：*"HSP70 Modulates FOXO3a Phosphorylation and Subcellular Localization in Cancer Cells"*
**作者**：Tzivion, G. et al.
**摘要**：该文献报道了HSP70通过调控AKT信号通路影响FOXO3a(FKHRL1)的Ser315磷酸化水平，进而影响其促凋亡功能。实验中采用Phospho-Ser315抗体检测了不同应激条件下该位点的磷酸化状态。
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**备注**：上述文献为示例，实际引用需根据具体研究内容检索PubMed或Sci-Hub获取原文。若需近期文献，建议使用关键词“FOXO3a Ser315 phosphorylation antibody”在数据库进一步筛选。
The FKHRL1 (Phospho-Ser315) antibody is designed to detect Forkhead box protein O3 (FoxO3a), a member of the Forkhead family of transcription factors, specifically when phosphorylated at serine 315. FoxO3a plays a critical role in regulating cellular processes such as apoptosis, cell cycle arrest, oxidative stress resistance, and DNA repair. Its activity is tightly controlled by post-translational modifications, including phosphorylation. The PI3K/Akt signaling pathway phosphorylates FoxO3a at Ser315 (and other residues), triggering its nuclear exclusion and binding to 14-3-3 proteins, thereby inhibiting its transcriptional activity. Dysregulation of FoxO3a phosphorylation is linked to cancer, aging, and metabolic disorders.
The FKHRL1 (Phospho-Ser315) antibody is a valuable tool for studying FoxO3a activation status in response to growth factors, insulin, or oxidative stress. It is commonly used in techniques like Western blotting, immunofluorescence, and immunohistochemistry to assess phosphorylation-dependent FoxO3a localization and function. Researchers employ this antibody to explore connections between FoxO3a signaling and diseases, such as tumor progression (where reduced nuclear FoxO3a correlates with poor prognosis) or neurodegenerative conditions. Specificity is often validated using knockout controls or phosphatase-treated samples. Understanding FoxO3a phosphorylation dynamics aids in developing therapeutic strategies targeting the PI3K/Akt/FoxO pathway.
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