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- W2003281056 abstract "Measles virus (MV) nucleoprotein (N) is a cytosolic protein that is released into the extracellular compartment after apoptosis and/or secondary necrosis of MV-infected cells in vitro . Thus, MV-N becomes accessible to inhibitory cell-surface receptors: Fc γ RIIB and an uncharacterized nucleoprotein receptor (NR). MV-N is composed of two domains: N CORE (aa 1–400) and N TAIL (aa 401–525). To assess the contribution of MV-N domains and of these two receptors in suppression of cell proliferation, a human melanoma HT144 cell line expressing (HT144IIB1) or lacking Fc γ RIIB1 was used as a model. Specific and exclusive N CORE –Fc γ RIIB1 and N TAIL –NR interactions were shown. Moreover, N TAIL binding to human NR predominantly led to suppression of cell proliferation by arresting cells in the G 0 /G 1 phases of the cell cycle, rather than to apoptosis. N CORE binding to HT144IIB1 cells primarily triggered caspase-3 activation, in contrast to HT144IIB1/IC − cells lacking the Fc γ RIIB1 intra-cytoplasmic tail, thus demonstrating the specific inhibitory effect of the N CORE –Fc γ RIIB1 interaction. MV-N- and N CORE -mediated apoptosis through Fc γ RIIB1 was inhibited by the pan-caspase inhibitor zVAD-FMK, indicating that apoptosis was dependent on caspase activation. By using N TAIL deletion proteins, it was also shown that the region of N TAIL responsible for binding to human NR and for cell growth arrest maps to one of the three conserved boxes (Box1, aa 401–420) found in N of Morbilliviruses . This work unveils novel mechanisms by which distinct domains of MV-N may display different immunosuppressive activities, thus contributing to our comprehension of the immunosuppressive state associated with MV infection. Finally, MV-N domains may be good tools to target tumour cell proliferation and/or apoptosis." @default.
- W2003281056 created "2016-06-24" @default.
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- W2003281056 date "2005-06-01" @default.
- W2003281056 modified "2023-09-25" @default.
- W2003281056 title "Measles virus nucleoprotein induces cell-proliferation arrest and apoptosis through NTAIL–NR and NCORE–FcγRIIB1 interactions, respectively" @default.
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- W2003281056 doi "https://doi.org/10.1099/vir.0.80791-0" @default.
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