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GSK3B — TNF

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: TNF → GSK3B (decreases, TNF Activity) Rottmann et al., Proc Natl Acad Sci U S A 2005*
  Evidence: The MYC protooncogene is frequently deregulated in human cancers. Here, by screening a kinase-directed library of small inhibitory RNAs, we identify glycogen synthase kinase 3beta (GSK3beta) as a gene whose inactivation potentiates TNF-related apoptosis-inducing ligand death receptor-mediated apoptosis specifically in MYC-overexpressing cells.

Text-mined interactions from Literome

Kim et al., J Biol Chem 2003 : Ectopic expression of GSK3 beta increased both basal and tumor necrosis factor alpha stimulated activities of MEKK1 in GSK3 beta ( -/- ) cells
Gupta et al., Biochim Biophys Acta 2004 : The effects of tumor necrosis factor-alpha (TNF-alpha) on insulin induced phosphorylation of protein kinase B-alpha (PKB-alpha) and downstream enzyme glycogen synthase kinase-3 beta ( GSK-3 beta ) was examined in HepG2 liver cells
Takada et al., J Biol Chem 2004 : Most surprisingly, TNF induced Akt activation also required the presence of GSK-3beta ... Overall, our results indicate that GSK-3beta plays a critical role in TNF signaling and in the signaling of other inflammatory stimuli and that its suppression can be exploited as a potential target to inhibit angiogenesis, proliferation, and survival of tumor cells
Vines et al., J Biol Chem 2006 : Novel anti-inflammatory role for glycogen synthase kinase-3beta in the inhibition of tumor necrosis factor-alpha- and interleukin-1beta induced inflammatory gene expression ... We observed that tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) treatment of primary cultures of human microvascular cells reduced net endogenous active GSK-3beta protein levels while inducing inflammatory cytokine ( IL-6 and monocyte chemoattractant protein-1 ( MCP-1 ) ) expression ... Overexpression of GSK-3beta in endothelial cells, in contrast, significantly inhibited ( by 70 %, p < 0.01 ) both TNF-alpha and IL-1beta induced expression of IL-6, MCP-1, and vascular cell adhesion molecule-1
Cuzzocrea et al., Clin Immunol 2006 (Arthritis, Experimental...) : Plasma levels of tumor necrosis factor (TNF)-alpha and the joint tissue levels of macrophage inflammatory protein (MIP)-1alpha and MIP-2 were also significantly reduced by GSK-3beta inhibition
Rickle et al., J Neurosci Res 2006 (Encephalitis...) : TNFalpha together with PTEN inhibition increased phosphorylation of Ser ( 473 ) Akt and Ser ( 9 ) GSK3beta
Ghosh et al., Endocrinology 2007 (Insulin Resistance) : Western blot analysis of L6 cell lysates demonstrated impaired insulin stimulated phosphorylation of Akt, serine/arginine-rich protein 40, and glycogen synthase kinase 3beta in response to TNFalpha and the short chain C6 ceramide analog ... Effects of TNFalpha and C6 on insulin stimulated phosphorylation of glycogen synthase kinase 3beta were prevented by myriocin and tautomycin, a PP1 inhibitor, further implicating a de novo ceramide-PP1 pathway
Gao et al., Inflamm Res 2009 (Myocardial Reperfusion Injury) : The present study defines the expression of Toll-like Receptor 2 (TLR2), and the modulatory role of Glycogen synthase kinase (GSK)-3beta inhibitor on TLR2/Nuclear Factor-kappa B (NF-kappaB) signaling following myocardial ischemia-reperfusion ( MI-R ) injury in rats
Yang et al., Cancer Cell 2009 (Cell Transformation, Neoplastic...) : Wu et al., in this issue of Cancer Cell, show that TNFalpha dependent NFkappaB activation induces COP9 signalosome mediated inhibition of GSK3beta and the SCF(beta-TRCP) ubiquitin ligase, thus leading to stabilization of the transcription factor Snail and promoting cell migration and metastasis
Cheng et al., Infect Immun 2009 (Inflammation) : Heat inactivated S. aureus activated GSK-3beta, and inhibiting GSK-3beta reduced TNF-alpha production as well as inducible NO synthase (iNOS)/NO biosynthesis ... These results suggest that GSK-3beta regulates heat inactivated S. aureus induced TNF-alpha and NO production in microglia mainly by activating NF-kappaB and probably by inhibiting IL-10