Roles of IKK-beta, IRF1, and p65 in the activation of chemokine genes by interferon-gamma.

Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research
David ShultzGeorge R Stark

Abstract

Activation of chemokine genes in response to interferon (IFN)-gamma or NF-kappaB is an important aspect of inflammation. Using the chemokine gene ip-10 in mouse embryonic fibroblast cells as an example, we show that the response to IFN-gamma is long lasting but secondary: initial STAT1 activation drives IRF1 synthesis, and IRF1 then binds to IFN-stimulated regulatory elements (ISREs) in the ip-10 promoter. The promoters of most IKK-beta-dependent IFN-stimulated genes (ISGs) also contain ISREs. In response to IFN-gamma, inhibitor of NF-kappaB (IkappaB) kinase beta (IKK-beta) is required to activate both newly synthesized IRF1 and the p65 subunit of NF-kappaB, which contributes to ip-10 expression by binding to kappaB sites in the ip-10 promoter, with little or no activation of classical NF-kappaB. In contrast to IFN-gamma, IL-1beta induces ip-10 expression rapidly but transiently, by activating classical NF-kappaB and increasing the synthesis of IRF1. Together, IL-1beta and IFN-gamma induce ip-10 synergistically. IFN-gamma does not affect the transient activation of classical NF-kappaB by IL-1beta and synergistic induction of ip-10 expression by IFN-gamma and IL-1beta occurs even after the activation of classical NF-kappaB has r...Continue Reading

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Citations

Apr 17, 2013·Infection and Immunity·Catherine E JaureguiRichard J Lamont
Mar 23, 2011·Infection and Immunity·Diana Diaz-ArevaloMarkus Kalkum
May 18, 2011·Molecular and Cellular Biology·Roshan J ThapaSiddharth Balachandran
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Dec 12, 2021·The Journal of Immunology : Official Journal of the American Association of Immunologists·Tae-Shin KimEui-Cheol Shin

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Methods Mentioned

BETA
electrophoresis
PCR
immunoprecipitation
ChIP
electrophoretic mobility shift assay
nuclear translocation

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