Visit our Expo - Redox and Inflammation signaling 2012

Session XIV : Transcriptional and translational control Poster XIV, 61
Synergy of p38 MAPK and Stat1 in Transcription
Iwona Sadzak, Barbara Schaljo and Pavel Kovarik
Max F.Perutz Laboratories, Department of Microbiology and Immunobiology,
University of Vienna, A-1030 Vienna, Austria
Both interferon (IFN) and stress signals are required for full activation of immune responses.
We and others have shown that the stress-activated p38 MAPK increases transcription by
Stat1, the key transcription factor of interferon signaling. Thus, the two signals synergistically
increase transcriptional responses under conditions of inflammation. We show here that
synergy of p38 MAPK with Stat1 generates unique gene expression patterns that are specific
for inflammatory conditions and allow identification of novel interferon-regulated genes. The
molecular basis for the synergy is unknown, but it does not depend on phosphorylation of
Stat1 by p38 MAPK.
We propose a working model for the synergy and describe the proteomic approach that we
employ to unravel the molecular mechanisms. We focus on the analysis of Stat1-containing
transcriptional complexes and p38-mediated modifications of their composition and/or
activity. We show that the amount of Stat1 protein on the promoters of target genes does not
change upon synchronous activation of IFNg and p38 MAPK pathway.Further we observe
that the association of CBP/p300 with Stat1 is unaffected by p38 MAPK activation.
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