Toll-like receptor–mediated cytokine production is differentially regulated by glycogen synthase kinase 3

1,134 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.

Toll-like receptors and cancer (2009, neutral): “shtml?what=graphic&gif=on&pathway_id=500219&source=7&output-format=graphic&ppage=1&genes_a=207">PI3K–Akt signalling pathway by TLR”
Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “…of Glucogen Synthase Kinase-3 (GSK3) in vivo, a kinase that is phosphorylated and inactivated by Akt, results in resistance to endotoxin shock (Martin et al., 2005), suggesting that inhibition of Akt will render mice more sensitive to LPS. Consistent with these observations, Akt…”
A Nurr1/CoREST transrepression pathway attenuates neurotoxic inflammation in activated microglia and astrocytes (2009, neutral): “Phosphorylation of Serine-468 (S468) in p65 is associated with negative regulation of NF-kB signaling (Buss et al., 2004) and can be mediated by GSK3b, which is activated following TLR4 stimulation in human monocytes ( Martin et al., 2005 ).”
Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases (2014, background): “Remarkably, administration of GSK3 inhibitors was sufficient to afford mice protection (survival) from an otherwise lethal dose of the inflammatory stimulant lipopolysaccharide used to model sepsis (Martin et al., 2005).”
NF-κB, an Active Player in Human Cancers (2014, positive): “Similarly, upon LPS stimulation, GSK-3 β has been shown to reduce nuclear phosphorylated CREB and their binding to CBP, making CBP more accessible to NF-κ B (48).”