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MAP3K8 — TNF

Text-mined interactions from Literome

Christoforidou et al., Molecular cancer 2004 (Leukemia, T-Cell...) : Animal and tissue culture studies have shown that Tpl2/Cot is involved in interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) production by T-cells contributing to T-cell proliferation
Das et al., J Biol Chem 2005 : In addition, we show that the activation of Tpl2 by TNF-alpha depends on signals transduced by both TRAF2 and RIP1
Jia et al., Anal Biochem 2006 (MAP Kinase Signaling System) : Cancer osaka thyroid (COT) is a member of the mitogen activated protein kinase kinase kinase family of enzymes and plays a pivotal role in tumor necrosis factor-alpha production in macrophages
Stafford et al., FEBS Lett 2006 : The protein kinase COT/Tpl2 is activated by interleukin-1 (IL-1), TNFalpha and lipopolysaccharide, and its activation by these agonists involves the IkappaB kinase beta (IKKbeta) catalysed phosphorylation of the p105 regulatory subunit
Hall et al., J Biol Chem 2007 (Arthritis, Rheumatoid...) : Moreover, Tpl2 is required for TNFalpha expression
Mielke et al., J Immunol 2009 (Listeriosis) : Surprisingly, TNF production in response to infection was not significantly impaired, even though Tpl2 has been implicated in the regulation of TNF
Ohnishi et al., J Dent Res 2010 (Alveolar Bone Loss...) : Furthermore, we found that Cot/Tp12 was involved in the induction of TNF-alpha mRNA expression in gingiva of mice with experimental periodontitis
Hirata et al., Biol Pharm Bull 2010 : Here, we studied the molecular mechanisms of Tpl2 mediated TNFalpha production using a potent Tpl2 kinase inhibitor, 1,7-naphtyridine-3-carbonitrile, and LPS stimulated RAW264.7 cells ... Although the TNFalpha mRNA level was not altered by either inhibitor, the Tpl2 inhibitor increased the nuclear TNFalpha mRNA level, while decreasing that in the cytoplasm
Yang et al., Mol Cell Biol 2012 : Unexpectedly, TPL-2 promoted soluble TNF production independently of IKK induced p105 phosphorylation and its ability to activate ERK, which has important implications for the development of anti-inflammatory drugs targeting TPL-2