Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

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

RESEARCH ARTICLES

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).

Read the Full Text


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Dendritic cell maturation: functional specialization through signaling specificity and transcriptional programming.
M. Dalod, R. Chelbi, B. Malissen, and T. Lawrence (2014)
EMBO J.
   Abstract »    Full Text »    PDF »
Inhibition of Transcription by B Cell Leukemia 3 (Bcl-3) Protein Requires Interaction with Nuclear Factor {kappa}B (NF-{kappa}B) p50.
P. E. Collins, P. A. Kiely, and R. J. Carmody (2014)
J. Biol. Chem. 289, 7059-7067
   Abstract »    Full Text »    PDF »
Models of signalling networks - what cell biologists can gain from them and give to them.
K. A. Janes and D. A. Lauffenburger (2013)
J. Cell Sci. 126, 1913-1921
   Abstract »    Full Text »    PDF »
Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages.
X. Chen, I. Barozzi, A. Termanini, E. Prosperini, A. Recchiuti, J. Dalli, F. Mietton, G. Matteoli, S. Hiebert, and G. Natoli (2012)
PNAS 109, E2865-E2874
   Abstract »    Full Text »    PDF »
EHMT1 Protein Binds to Nuclear Factor-{kappa}B p50 and Represses Gene Expression.
C.-K. Ea, S. Hao, K. S. Yeo, and D. Baltimore (2012)
J. Biol. Chem. 287, 31207-31217
   Abstract »    Full Text »    PDF »
Science Signaling Podcast: 22 February 2011.
A. Hoffmann and A. M. VanHook (2011)
Science Signaling 4, pc3
   Abstract »    Full Text »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882