Achieving Stability of Lipopolysaccharide-Induced NF-κB Activation

Author:

Covert Markus W.1,Leung Thomas H.1,Gaston Jahlionais E.1,Baltimore David1

Affiliation:

1. Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.

Abstract

The activation dynamics of the transcription factor NF-κB exhibit damped oscillatory behavior when cells are stimulated by tumor necrosis factor–α (TNFα) but stable behavior when stimulated by lipopolysaccharide (LPS). LPS binding to Toll-like receptor 4 (TLR4) causes activation of NF-κB that requires two downstream pathways, each of which when isolated exhibits damped oscillatory behavior. Computational modeling of the two TLR4-dependent signaling pathways suggests that one pathway requires a time delay to establish early anti-phase activation of NF-κB by the two pathways. The MyD88-independent pathway required Inferon regulatory factor 3–dependent expression of TNFα to activate NF-κB, and the time required for TNFα synthesis established the delay.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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