| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/100-1/300 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/20000 | Human,Mouse,Rat |
| Aliases | AXL; UFO; Tyrosine-protein kinase receptor UFO; AXL oncogene |
| Entrez GeneID | 558; |
| 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 | Synthesized peptide derived from human Axl around the phosphorylation site of Y691. |
| 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 Axl (Phospho-Tyr691) 抗体的3篇参考文献示例，涵盖其功能研究和应用场景：
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1. **文献名称**：*Axl Phosphorylation at Tyrosine 691 Promotes Tumor Cell Survival and Immune Evasion in Breast Cancer*
**作者**：Zhang Y et al.
**摘要**：本研究探讨了 Axl 在乳腺癌中 Tyr691 位点磷酸化对肿瘤细胞存活和免疫逃逸的影响。通过使用特异性抗体检测磷酸化水平，发现 Axl-Y691 磷酸化通过激活 PI3K/AKT 通路抑制凋亡，并促进 PD-L1 表达以逃避免疫监视。抑制该位点磷酸化可增强化疗敏感性和 T 细胞抗肿瘤活性。
2. **文献名称**：*Targeting Phosphorylated Axl (Y691) Suppresses Metastatic Prostate Cancer Progression*
**作者**：Holland SJ et al.
**摘要**：作者利用 Axl (Phospho-Tyr691) 抗体验证了该位点在前列腺癌转移中的关键作用。研究表明，Y691 磷酸化增强了 Axl 与 Gas6 配体的结合能力，驱动 EMT 和骨转移。通过小分子抑制剂阻断磷酸化可显著降低肿瘤侵袭性，为转移性前列腺癌提供了潜在治疗靶点。
3. **文献名称**：*Phosphorylation of Axl at Tyr691 Sustains STAT3 Signaling in Glioblastoma Stem Cells*
**作者**：Chen X et al.
**摘要**：本文揭示了胶质母细胞瘤干细胞中 Axl-Y691 磷酸化通过激活 STAT3 信号维持肿瘤干性。使用特异性抗体检测发现，磷酸化 Axl 与 STAT3 的核转位相关，促进肿瘤自我更新和放化疗抵抗。靶向该位点可抑制肿瘤干细胞特性并改善预后。
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**注**：以上文献为示例，实际引用需根据具体研究检索 PubMed 或 Web of Science 等数据库。建议使用关键词“Axl Phospho-Tyr691”或“Axl Y691 phosphorylation”查找最新研究。
The Axl (Phospho-Tyr691) antibody is a specialized tool used to study the activation status of Axl, a receptor tyrosine kinase belonging to the TAM family (Tyro3. Axl, MerTK). Axl plays critical roles in cellular processes such as proliferation, survival, migration, and immune regulation. Its activation typically occurs through binding to the ligand Gas6. leading to receptor dimerization, autophosphorylation, and downstream signaling. Phosphorylation at tyrosine residue 691 (Tyr691) is a key event in Axl activation, serving as a docking site for adaptor proteins that mediate signaling pathways like PI3K/AKT, MAPK/ERK, and STAT3.
This antibody specifically detects Axl when phosphorylated at Tyr691. making it valuable for investigating Axl’s functional state in physiological and pathological contexts. Dysregulated Axl signaling is implicated in cancer progression, metastasis, and therapy resistance, as well as inflammatory and autoimmune diseases. Researchers use the Axl (Phospho-Tyr691) antibody in techniques like Western blotting, immunohistochemistry, and flow cytometry to assess Axl activation in cell lines, tissues, or preclinical models. Its application aids in understanding Axl’s role in disease mechanisms and evaluating therapeutic strategies targeting Axl phosphorylation, such as small-molecule inhibitors or monoclonal antibodies. Proper controls (e.g., phosphorylation-blocking treatments or Axl-deficient samples) are essential to ensure antibody specificity.
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