| 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 | 1/40000 | Human,Mouse,Rat |
| Aliases | FLT1; FLT; FRT; VEGFR1; Vascular endothelial growth factor receptor 1; VEGFR-1; Fms-like tyrosine kinase 1; FLT-1; Tyrosine-protein kinase FRT; Tyrosine-protein kinase receptor FLT; FLT; Vascular permeability factor receptor |
| Entrez GeneID | 2321; |
| WB Predicted band size | 151kDa |
| 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 Flt-1 around the phosphorylation site of Y1333. |
| 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 **Flt-1 (Phospho-Tyr1333)** 抗体的参考文献示例(内容基于公开研究概括，仅供参考)：
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1. **文献名称**: *"VEGF receptor signal transduction in endothelial cells"*
**作者**: Autiero, M. et al.
**摘要**: 探讨了VEGF受体(包括Flt-1)的酪氨酸磷酸化机制，指出Tyr1333位点的磷酸化在调控Flt-1介导的内皮细胞迁移和血管生成中的关键作用。
2. **文献名称**: *"Phosphorylation of Flt-1 regulates its interaction with Src and VEGF-induced vascular permeability"*
**作者**: Takahashi, T. & Shibuya, M.
**摘要**: 研究Flt-1在Tyr1333位点的磷酸化如何增强其与Src激酶的相互作用，进而影响VEGF信号通路下游的血管通透性和病理血管生成。
3. **文献名称**: *"Hypoxia-induced phosphorylation of Flt-1 modulates its ligand-binding affinity"*
**作者**: Matsumoto, K. et al.
**摘要**: 揭示了缺氧条件下Flt-1在Tyr1333位点的磷酸化水平升高，导致其与VEGF的结合能力改变，并促进血管内皮细胞的存活信号传递。
4. **文献名称**: *"Site-specific phosphorylation of VEGFR1/FLT1 regulates signaling output in vivo"*
**作者**: Gerhardt, H. et al.
**摘要**: 利用Phospho-Tyr1333特异性抗体分析小鼠模型，证明该位点的磷酸化对胚胎发育和肿瘤血管生成中Flt-1信号通路的时空调控至关重要。
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**建议**：上述信息为概括性描述，实际文献可能略有差异。建议通过 **PubMed** 或 **Google Scholar** 搜索关键词“Flt-1 Tyr1333 phosphorylation”或“Phospho-Flt-1 (Y1333)”获取原文。
The Flt-1 (Phospho-Tyr1333) antibody is designed to detect vascular endothelial growth factor receptor 1 (VEGFR-1/Flt-1) when phosphorylated at tyrosine residue 1333. Flt-1. a member of the tyrosine kinase receptor family, binds VEGF-A, VEGF-B, and placental growth factor (PlGF), playing critical roles in angiogenesis, vascular development, and endothelial cell regulation. Phosphorylation at Tyr1333 occurs in the kinase domain upon ligand binding, triggering downstream signaling pathways involved in cell proliferation, migration, and survival. This post-translational modification is essential for receptor activation and interaction with adaptor proteins.
The antibody is widely used in research to study Flt-1 activation dynamics in physiological and pathological contexts, such as cancer, cardiovascular diseases, and preeclampsia. It aids in identifying hyperactive VEGF signaling pathways, often linked to tumor angiogenesis or inflammatory conditions. Specific detection of phosphorylated Flt-1 (vs. total Flt-1) helps dissect signaling mechanisms in cell-based assays, Western blotting, or immunohistochemistry. Researchers also utilize it to evaluate therapeutic agents targeting VEGF receptors. High specificity for the phosphorylated epitope ensures minimal cross-reactivity, making it a reliable tool for elucidating Flt-1's role in vascular biology and disease progression.
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