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- W2106279075 abstract "Death receptor-mediated apoptosis is potently inhibited by viral FLIP (FLICE/caspase 8 inhibitory protein), which is composed of two tandemly repeated death effector domains (DEDs), through reduced activation of procaspase 8. Here, we show that equine herpesvirus 2-encoded viral FLIP E8 enhances Wnt/β-catenin signaling in a variety of cell lines. E8 was shown to strikingly augment Wnt3a signaling, as shown both in a luciferase assay for T-cell factor/β-catenin and through induction of endogenous cyclin D1. The effect of E8 was independent of its direct binding activity with DED-containing signaling molecules, including caspase 8 and FADD, in death receptor-mediated apoptosis. E8 enhanced Wnt signaling downstream of stabilized β-catenin, while a long form of cellular FLIP (c-FLIPL) enhanced stabilization of β-catenin in 293T cells. Consequently, coexpression of E8 and c-FLIPL synergistically increased Wnt signaling in 293T cells. Moreover, E8-mediated stimulation of Wnt signaling induced dramatic growth retardation in untransformed cell lines but not in transformed cell lines. Thus, viral FLIP E8 not only inhibits death receptor-mediated apoptosis but also enhances Wnt signaling pathways that are closely related to those of both ontogenesis and oncogenesis." @default.
- W2106279075 created "2016-06-24" @default.
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- W2106279075 date "2005-11-01" @default.
- W2106279075 modified "2023-10-03" @default.
- W2106279075 title "Viral FLIP Enhances Wnt Signaling Downstream of Stabilized β-Catenin, Leading to Control of Cell Growth" @default.
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- W2106279075 doi "https://doi.org/10.1128/mcb.25.21.9249-9258.2005" @default.
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