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NF-κB and IRF pathways: cross-regulation on target genes promoter level

The NF-κB and IRF transcription factor families are major players in inflammation and antiviral response and act as two major effectors of the innate immune response (IIR). The regulatory mechanisms of activation of these two pathways and their interactions during the IIR are only partially known. O...

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Published in:BMC genomics 2015-04, Vol.16 (1), p.307-307, Article 307
Main Authors: Iwanaszko, Marta, Kimmel, Marek
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Language:English
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cited_by cdi_FETCH-LOGICAL-c469t-7bfe07b7ed07cb87a735831419d326c57f62df51f68955f55575a38cdd30c9a3
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description The NF-κB and IRF transcription factor families are major players in inflammation and antiviral response and act as two major effectors of the innate immune response (IIR). The regulatory mechanisms of activation of these two pathways and their interactions during the IIR are only partially known. Our in silico findings report that there is cross-regulation between both pathways at the level of gene transcription regulation, mediated by the presence of binding sites for both factors in promoters of genes essential for these pathways. These findings agree with recent experimental data reporting crosstalk between pathways activated by RIG-I and TLR3 receptors in response to pathogens. We present an extended crosstalk diagram of the IRF - NF-κB pathways. We conclude that members of the NF-κB family may directly impact regulation of IRF family, while IRF members impact regulation of NF-κB family rather indirectly, via other transcription factors such as AP-1 and SP1.
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subjects 3' Untranslated Regions
Animals
Binding Sites
Humans
Interferon Regulatory Factors - genetics
Interferon Regulatory Factors - metabolism
NF-kappa B - genetics
NF-kappa B - metabolism
Promoter Regions, Genetic
Signal Transduction
Toll-Like Receptor 3 - genetics
Toll-Like Receptor 3 - metabolism
Transcription Factors - chemistry
Transcription Factors - metabolism
title NF-κB and IRF pathways: cross-regulation on target genes promoter level
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