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The Itch ubiquitin ligase is required for KSHV RTA induced vFLIP degradation.

Abstract：

:Expression of Kaposi's sarcoma herpesvirus vFLIP, a potent activator of NFkB signaling, promotes latency. Inhibition of NFkB signaling promotes lytic reactivation. We previously reported that lytic inducer, RTA, inhibits vFLIP induced NFkB signaling by inducing the degradation of vFLIP via the proteasome. Here we report that the cellular ubiquitin ligase, Itch, is required for RTA induced degradation of vFLIP. Expression of either Itch targeting shRNA or a dominant negative mutant of the ubiquitin ligase both increased the stability of vFLIP in the presence of RTA. Itch potently ubiquitinated vFLIP in vivo and in vitro. We provide evidence for interaction between RTA, vFLIP and Itch and we identified an RTA resistant mutant of vFLIP that is unable to interact with Itch. These observations contribute to our understanding of how RTA counteracts the activities of vFLIP.

journal_name

Virology

journal_title

Virology

authors

Chmura JC,Herold K,Ruffin A,Atuobi T,Fabiyi Y,Mitchell AE,Choi YB,Ehrlich ES

doi

10.1016/j.virol.2016.11.016

subject

Has Abstract

pub_date

2017-01-15 00:00:00

pages

119-126

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(16)30370-1

journal_volume

501

pub_type

杂志文章

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