EphA2 (D4A2) XP ® Rabbit mAb from Cell Signaling Technology

EphA2 has been shown to be hyperactivated in patients treated with 5-fluorouracil (5FU) chemotherapy, correlating with lower disease-free survival. Silencing EphA2, along with c-MET, resulted in a significant decrease in the invasive and tumorigenic potential of triple-negative breast cancer cells, indicating that targeting EphA2 may enhance treatment efficacy in this context (mitra2023).

EphA2 functions as a receptor on neutrophils that enhances antifungal activity during oropharyngeal candidiasis. It is involved in the accumulation of phagocytes in the oral mucosa and activates the MEK-ERK signaling pathway, which increases reactive oxygen species production, thereby augmenting the neutrophil's ability to kill Candida albicans (swiderga2019).

Yes, EphA2 phosphorylation has been linked to melanoma cell migration and the formation of lamellipodia through the oncogenic MAPK pathway. Specifically, the BRAF oncogene induces EphA2 phosphorylation, which is necessary for cell migration in melanoma cells, highlighting its role in cancer metastasis (yasuta2024).

Research has indicated that sequential treatment with anti-EGFR and anti-VEGF antibodies in RAS wild-type metastatic colorectal cancer leads to reduced EphA2 expression and phosphorylation, suggesting that EphA2 may be a relevant target in optimizing therapeutic strategies for this cancer type ().