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Inducible cAMP early repressor (ICER) is a novel regulator of RIG-I mediated IFN-β production.

Abstract：

:Antiviral responses can be triggered by the cytoplasmic RNA helicase RIG-I that binds to viral RNA. RIG-I-mediated signaling stimulates the transcription factors IRF3 and NF-κB and their activation mechanisms have been intensively studied. Here we examined Sendai virus (SV)-mediated activation of the transcription factor CREB and the role of its feedback repressor ICER in production of endogenous antiviral proteins. We show that SV infection and the mitochondrial adapter protein MAVS promote CREB phosphorylation that is dependent upon p38 MAPK and MK2. ICER is induced by CREB and acts as a feedback repressor of CRE-dependent transcription. We found that SV infection stimulated induction of ICER mRNA and protein expression. Surprisingly, ectopic expression and siRNA-mediated knockdown of ICER revealed that ICER is a positive regulator of the production of antiviral IFN-β and IP10 during SV infection. In contrast, ICER did not affect SV-elicited phosphorylation of IRF3, NF-κB or ATF2/c-Jun, transcription factors governing IFN-β and IP10 synthesis. However, expression of ICER increased total IRF3 protein levels during SV infection. These results point to a novel role of ICER in antiviral immune signaling acting to increase levels of antiviral effectors.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Johnsen IB,Bergstroem B,Stiberg KA,Thommesen L,Anthonsen MW

doi

10.1016/j.cellsig.2013.05.014

subject

Has Abstract

pub_date

2013-09-01 00:00:00

pages

1804-12

issue

9

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(13)00139-3

journal_volume

25

pub_type

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