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Sci. Signal., 22 February 2011
Vol. 4, Issue 161, p. ra11
[DOI: 10.1126/scisignal.2001501]


Editor's Summary

NF-{kappa}B Interferes
Signaling pathways triggered by pattern recognition receptors elicit gene expression programs that culminate in antiviral or proinflammatory responses. Critical to these are members of the nuclear factor {kappa}B (NF-{kappa}B) and interferon regulatory factor (IRF) families of transcription factors, which bind to {kappa}B sites and interferon response elements (IREs), respectively, in their target genes. In addition to transcriptional activators, the NF-{kappa}B family of proteins contains p50, which forms homodimers that act as competitive repressors at {kappa}B sites. Noting the importance of transcriptional repressors in preventing inappropriate gene expression, Cheng et al. investigated roles for p50 in immune responses. They showed that p50 homodimers bound to and regulated a subset of IREs that were guanine-rich (G-IREs). Homodimers of p50 set the threshold for the activation of genes by competing with IRFs for binding to G-IREs, effectively acting as promoter "gates" to restrict gene expression to specific stimuli. Together, these data provide evidence of cross-regulation between the main sets of transcription factors that coordinate innate immune responses.

Citation: C. S. Cheng, K. E. Feldman, J. Lee, S. Verma, D.-B. Huang, K. Huynh, M. Chang, J. V. Ponomarenko, S.-C. Sun, C. A. Benedict, G. Ghosh, A. Hoffmann, The Specificity of Innate Immune Responses Is Enforced by Repression of Interferon Response Elements by NF-{kappa}B p50. Sci. Signal. 4, ra11 (2011).

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