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2014 ; 8
(5
): 1308-17
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IRF5:RelA interaction targets inflammatory genes in macrophages
#MMPMID25159141
Saliba DG
; Heger A
; Eames HL
; Oikonomopoulos S
; Teixeira A
; Blazek K
; Androulidaki A
; Wong D
; Goh FG
; Weiss M
; Byrne A
; Pasparakis M
; Ragoussis J
; Udalova IA
Cell Rep
2014[Sep]; 8
(5
): 1308-17
PMID25159141
show ga
Interferon Regulatory Factor 5 (IRF5) plays a major role in setting up an
inflammatory macrophage phenotype, but the molecular basis of its transcriptional
activity is not fully understood. In this study, we conduct a comprehensive
genome-wide analysis of IRF5 recruitment in macrophages stimulated with bacterial
lipopolysaccharide and discover that IRF5 binds to regulatory elements of highly
transcribed genes. Analysis of protein:DNA microarrays demonstrates that IRF5
recognizes the canonical IRF-binding (interferon-stimulated response element
[ISRE]) motif in vitro. However, IRF5 binding in vivo appears to rely on its
interactions with other proteins. IRF5 binds to a noncanonical composite
PU.1:ISRE motif, and its recruitment is aided by RelA. Global gene expression
analysis in macrophages deficient in IRF5 and RelA highlights the direct role of
the RelA:IRF5 cistrome in regulation of a subset of key inflammatory genes. We
map the RelA:IRF5 interaction domain and suggest that interfering with it would
offer selective targeting of macrophage inflammatory activities.