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- W1996017816 abstract "Protein kinase D1 (PKD1 or PKCμ) is a serine/threonine kinase that contributes to malignant progression. Although B and T cells express multiple PKCs, modulation of PKC in association with EBV has not been evaluated. In this study we examined the effects of PKD1 as a cellular target of EBV latent membrane protein-1 (LMP1) on the response of malignant B cells to rituximab and doxorubicin. LMP1 up-regulated PKD1 in malignant B cells but not in T cells. Interestingly, LMP1 stabilized PKD1 protein through direct interaction, which contributed to the survival of malignant B cells. In the absence of PKD1, LMP1 was unable to up-regulate Mcl-1. Also, PH domain and activation loop of PKD1 was critical for LMP1-mediated cell survival. PKD1 knockdown was found to be an efficient strategy to overcome resistance caused by LMP1 expression. Therefore, PKD1 could be a molecular target for therapeutic intervention in EBV-associated B cell lymphoma treatment." @default.
- W1996017816 created "2016-06-24" @default.
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- W1996017816 date "2014-06-25" @default.
- W1996017816 modified "2023-09-28" @default.
- W1996017816 title "PKD1 is critical for Epstein–Barr virus LMP1-induced protection of malignant B cells from cell death induced by rituximab" @default.
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- W1996017816 doi "https://doi.org/10.3109/10428194.2014.911860" @default.
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