Role of the transcription factor C/EBPδ in a regulatory circuit that discriminates between transient and persistent Toll-like receptor 4-induced signals View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2009-03-08

AUTHORS

Vladimir Litvak, Stephen A. Ramsey, Alistair G. Rust, Daniel E. Zak, Kathleen A. Kennedy, Aaron E. Lampano, Matti Nykter, Ilya Shmulevich, Alan Aderem

ABSTRACT

The innate immune system is like a double-edged sword: it is absolutely required for host defense against infection, but when uncontrolled, it can trigger a plethora of inflammatory diseases. Here we use systems-biology approaches to predict and confirm the existence of a gene-regulatory network involving dynamic interaction among the transcription factors NF-kappaB, C/EBPdelta and ATF3 that controls inflammatory responses. We mathematically modeled transcriptional regulation of the genes encoding interleukin 6 and C/EBPdelta and experimentally confirmed the prediction that the combination of an initiator (NF-kappaB), an amplifier (C/EBPdelta) and an attenuator (ATF3) forms a regulatory circuit that discriminates between transient and persistent Toll-like receptor 4-induced signals. Our results suggest a mechanism that enables the innate immune system to detect the duration of infection and to respond appropriately. More... »

PAGES

437-443

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ni.1721

DOI

http://dx.doi.org/10.1038/ni.1721

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024867765

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/19270711


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