Abstract:
:Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) vFLIP, a latent gene of KSHV, was first identified as a FLICE-inhibitory protein (FLIP) protecting cells from apoptosis. The vFLIP protein has been shown to activate the NF-κB signaling involved in spindle morphology formation both in HUVECs infected with KSHV and Kaposi's sarcoma (KS) itself. In this study, we independently established stably vFLIP-expressing cells and showed that they exhibited upregulated NF-κB family protein expression independent of the ability of IKKs to bind vFLIP. Further, vFLIP induced upregulation of IKKε, phosphorylation of RelA at Ser468 (p-RelA S468) and nuclear localization of Re1A concomitant with spindle morphology formation, and these effects were reversed by knockdown of IKKε and treatment with Bay-11. Overexpression of IKKε alone also showed spindle morphology formation with p-RelA S468. In conclusion, the spindle cell morphology in KS should be induced by RelA activation (p-RelA S468) by IKKε upregulation in vFLIP-expressing EA hy926 cells.
journal_name
Virologyjournal_title
Virologyauthors
Yang Z,Honda T,Ueda Kdoi
10.1016/j.virol.2018.07.007subject
Has Abstractpub_date
2018-09-01 00:00:00pages
106-121eissn
0042-6822issn
1096-0341pii
S0042-6822(18)30209-5journal_volume
522pub_type
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