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Abstract

In replicating LCLs, both isoforms of RAB11FIP1 exhibited increased expression compared to latent LCLs. Notably, both RAB11FIP1C and RAB11FIPB were found to enhance BZLF1 expression, and this effect was shown to be dependent on the C2 domain. The increasing effects of RAB11FIP1C on BZLF1 were observed regardless of any transcriptional or proteomic changes induced by RAB11FIP1. Furthermore, the dynamic shift in the localization of RAB11FIP1 from the perinuclear region to the plasma membrane may contribute to an increased presence of EGFR in the plasma membrane. Consequently, the activation of MAPK/ERK pathway by EGF triggered by EGF, facilitating the replication of EBV. Moreover, the overexpression of RAB11FIP1 in replicating LCLs has the potential to enhance ERK phosphorylation and activate RAS, leading to the activation of the MAPK pathway and, consequently, an enhancement of EBV replication. These interconnected findings underscore the multifaceted role of RAB11FIP1 in influencing BZLF1 expression, cellular localization, EGFR signaling, and downstream MAPK pathway activation, ultimately contributing to the replication of EBV in LCLs.