Achieving Stability of Lipopolysaccharide-Induced NF-κB Activation

By Markus W. Covert, Thomas H. Leung, Jahlionais E. Gaston, David Baltimore. Science, 2005

600 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Transcriptional control of the inflammatory response (2009, background): “However, positive feed-forward mechanisms might ensure the sustained activation of these transcription factors and their participation in subsequent waves of gene induction; for example, the production of tumour necrosis factor ( TNF ) triggered by LPS stimulation seems to be crucial for autocrine s”
Integrating cell-signalling pathways with NF-κB and IKK function (2007, background): “This is a result of IRF3 -dependent TNFα synthesis leading to a positive feedback loop that restimulates IKK activit”
Transcriptional regulation via the NF-κB signaling module (2006, background): “Initial studies have identified A20 as a critical negative feedback regulator of TNF-induced IKK (Lee et al., 2000; Werner et al., 2005), whereas the LPS-induced IKK activity involves positive feedback regulation via an autocrine TNF loop (Covert et al., 2005; Werner et al., 2005).”
NF-κB and the immune response (2006, background): “Adding further complexity, it has recently been suggested that TLR4, but not TLR3, TRIFdependent NF-kB activation is largely due to IRF3induced TNFa rather than to direct signaling to IKK (Covert et al., 2005; Werner et al., 2005).”