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Sci. Signal., 22 February 2011
Vol. 4, Issue 161, p. ra11
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 B (NF-B) and interferon regulatory factor (IRF) families of transcription factors, which bind to B sites and interferon response elements (IREs), respectively, in their target genes. In addition to transcriptional activators, the NF-B family of proteins contains p50, which forms homodimers that act as competitive repressors at 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-B p50. Sci. Signal.4, ra11 (2011).