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KSHV vIRF4 enhances BCL6 transcription via downregulation of IRF4 expression.

Abstract：

:Primary effusion lymphoma (PEL), strongly linked with latent infection of Kaposi's sarcoma-associated herpesvirus (KSHV), constitutively expresses cellular interferon regulatory factor 4 (IRF4) while suppressing the expression of B cell lymphoma 6 (BCL6). Recently, it was shown that IRF4, a key transcriptional repressor of BCL6, might be a pivotal regulator of KSHV for balancing between latency and its reactivation in PEL cells. However, the action of the BCL6-IRF4 transcription factor axis during KSHV's life cycle is not clear. Herein we found that the KSHV lytic protein viral interferon regulatory factor 4 (vIRF4) dramatically enhanced the transcriptional activity of the BCL6 through the inhibition of its negative regulator IRF4. Using a chromatin immunoprecipitation (ChIP) assay, we further showed that vIRF4 bound to the specific promoter region of IRF4, contributing to a dramatic suppression of IRF4 gene expression. Correspondingly, we also found BCL6 expression to be positively and inversely correlated with vIRF4 and IRF4 expression, respectively, during KSHV reactivation. Finally, we observed that these processes require efficient KSHV lytic replication. Thus, our findings suggest a crucial role of the BCL6-IRF4 axis in triggering the transition between KSHV latency and lytic reactivation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Yu HR,Kim YJ,Lee HR

doi

10.1016/j.bbrc.2018.01.154

subject

Has Abstract

pub_date

2018-02-19 00:00:00

pages

1128-1133

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(18)30177-3

journal_volume

496

pub_type

杂志文章

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