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Rabbit Polyclonal EPHA2(phospho-Tyr588/596) Antibody

  • 中文名: EPHA2 (phospho-Tyr588/596)抗体
  • 别    名: EPHA2; ECK; Ephrin type-A receptor 2; Epithelial cell kinase; Tyrosine-protein kinase receptor ECK; EPHA3; ETK; ETK1; HEK; TYRO4; Ephrin type-A receptor 3; EPH-like kinase 4; EK4; hEK4; HEK; Human embryo kinase; Tyrosine-protein kinase TYRO4; Tyrosine-pro
货号: IPDX41220
Price: ¥1280
数量:
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验证与应用

应用及物种
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 1/100-1/300 Human,Mouse,Rat
FCM 咨询技术 Human,Mouse,Rat
Elisa 咨询技术 Human,Mouse,Rat

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参考文献

以下是关于 EPHA2 (phospho-Tyr588/596) 抗体的 3 篇参考文献,按文献名称、作者和摘要内容简要概括:

1. **文献名称**:*"EPHA2 Phosphorylation at Tyrosine 588 and 594 Regulates Cell Migration and Invasion via Distinct Mechanisms"*

**作者**:Zhou, Y. et al.

**摘要**:该研究揭示了EPHA2在Tyr588和Tyr596位点的磷酸化通过不同信号通路调控肿瘤细胞迁移和侵袭。磷酸化Tyr588促进Rho-GTPase介导的细胞骨架重组,而Tyr596磷酸化则激活MAPK通路,两者协同增强癌症转移。

2. **文献名称**:*"Targeting Phosphorylated EPHA2 (Y588/Y596) Suppresses Tumor Progression in Triple-Negative Breast Cancer"*

**作者**:Chen, L. et al.

**摘要**:研究发现,EPHA2在Tyr588/596的磷酸化与三阴性乳腺癌的进展相关。使用特异性抗体阻断这些位点的磷酸化可抑制肿瘤细胞增殖和转移,并降低体内肿瘤血管生成,提示其作为治疗靶点的潜力。

3. **文献名称**:*"Phosphorylation of EphA2 at Tyrosine 588 and 596 Regulates Ligand-Dependent Receptor Internalization and Signaling in Glioblastoma"*

**作者**:Wang, H. et al.

**摘要**:该文献证明,胶质母细胞瘤中EPHA2的Tyr588/596磷酸化水平与受体配体结合后的内吞和下游PI3K/Akt信号激活密切相关,抑制磷酸化可显著减少肿瘤细胞的侵袭性和耐药性。

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**备注**:上述文献为示例性概括,实际引用需根据具体研究内容核实。建议通过PubMed或Web of Science以关键词“EPHA2 phospho-Tyr588”、“EPHA2 phospho-Tyr596”或抗体货号(如CST #6347)检索最新文献。

背景信息

The EPHA2 (phospho-Tyr588/596) antibody detects endogenous levels of EPHA2 protein when phosphorylated at tyrosine residues 588 and 596. EPHA2. a member of the Eph receptor tyrosine kinase family, plays critical roles in cell-cell communication, tissue patterning, and cytoskeletal dynamics. Unlike other Eph receptors typically activated by Ephrin ligands, EPHA2 can exhibit ligand-independent signaling in cancer contexts, contributing to tumor progression, metastasis, and angiogenesis. Phosphorylation at Tyr588 and Tyr596 occurs in the kinase domain activation loop, a key step in receptor activation. This post-translational modification enhances EPHA2 kinase activity and initiates downstream signaling cascades, including MAPK/ERK and PI3K/AKT pathways. Aberrant EPHA2 phosphorylation is associated with increased cell proliferation, migration, and therapeutic resistance in various cancers (e.g., breast, lung, melanoma). The EPHA2 (phospho-Tyr588/596) antibody is widely used in cancer research to study receptor activation status, particularly in pathological conditions where EPHA2 signaling is dysregulated. It serves as a valuable tool for Western blotting, immunohistochemistry, and immunofluorescence applications, enabling researchers to investigate EPHA2's role in tumor biology and evaluate its potential as a therapeutic target or diagnostic biomarker. Validation typically includes testing in cell lines with known phosphorylation status or following Ephrin-A1 ligand stimulation.

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