Journal
VIROLOGY
Volume 522, Issue -, Pages 106-121Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2018.07.007
Keywords
VFLIP; NF-kappa Bs; Spindle morphology; IKK epsilon; RelA; p-RelA 5468
Categories
Funding
- Japan Agency for Medical Research and Development (AMED) [JP16fk0410107, JP17fk0410207, JP18fk0410007]
Ask authors/readers for more resources
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-kappa B 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-kappa B family protein expression independent of the ability of IKK epsilon to bind vFLIP. Further, vFLIP induced upregulation of IKK epsilon, phosphorylation of RelA at Ser468 (p-RelA S468) and nuclear localization of RelA concomitant with spindle morphology formation, and these effects were reversed by knockdown of IKK epsilon and treatment with Bay-11. Overexpression of IKK epsilon alone also showed spindle morphology formation with p-RelA 5468. In conclusion, the spindle cell morphology in KS should be induced by RelA activation (p-RelA 5468) by IKK epsilon upregulation in vFLIP-expressing EA hy926 cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available