Gene interactions and pathways from curated databases and text-mining

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IRF6 — MAP3K8

Text-mined interactions from Literome

Eliopoulos et al., EMBO J 2002 (Inflammation) : Thus, LPS stimulated Tpl2 ( -/- ) macrophages express low levels of COX-2 and PGE2, compared with wild-type Tpl2 ( +/+ ) cells
Caivano et al., J Biol Chem 2003 : A tyrosine kinase activity is involved in Cot activation by LPS ... Furthermore, 15-deoxy-Delta12,14-prostaglandin J2 also inhibited the LPS induced Cot in vitro ... Considering these data, we propose that the inhibition of LPS induced Cot activation is one mechanism by which 15-deoxy-Delta12,14-prostaglandin J2 acts as an anti-inflammatory
Lang et al., Mol Cell Biol 2004 : Although the majority of TPL-2 in these cells was complexed with ABIN-2, the pool of TPL-2 which could activate MEK after LPS stimulation was not, and LPS activation of TPL-2 was found to correlate with its release from ABIN-2
Beinke et al., Mol Cell Biol 2004 (MAP Kinase Signaling System) : The MEK kinase TPL-2 ( also known as Cot ) is required for lipopolysaccharide (LPS) activation of the extracellular signal regulated kinase ( ERK ) mitogen activated protein ( MAP ) kinase cascade in macrophages and consequent upregulation of genes involved in innate immune responses ... Expression of a p105 point mutant, which is not susceptible to signal induced proteolysis, in RAW264.7 macrophages impairs LPS induced release of TPL-2 from p105 and its subsequent activation of MEK ... Consistently, pharmacological blockade of IKK inhibits LPS induced release of TPL-2 from p105 and TPL-2 activation ... These data show that IKK induced p105 proteolysis is essential for LPS activation of TPL-2 , thus revealing a novel function of IKK in the regulation of the ERK MAP kinase cascade
Cho et al., J Biol Chem 2005 : We conclude that Tpl2 phosphorylation at Thr ( 290 ) is induced by LPS , depends on IKKbeta, and is required for the physiological activation of Tpl2 by external signals
Babu et al., Biochim Biophys Acta 2006 : Recent studies demonstrate that the NF-kappaB1 precursor protein p105 functions as an inhibitor of Tpl2 and that the LPS stimulated Tpl2 activation requires p105 degradation
Robinson et al., Mol Cell Biol 2007 : LPS activation of ERK requires TPL-2 release from associated NF-kappaB1 p105, which blocks TPL-2 access to its substrate, the ERK kinase MEK ... Thus, induction of TPL-2 MEK kinase activity by LPS stimulation of macrophages requires TPL-2 phosphorylation on S400, in addition to its release from NF-kappaB1 p105
Zhang et al., Cell Signal 2009 (MAP Kinase Signaling System) : Lithium also promotes the activation of Tpl2 and ERK by the TLR4 ligand LPS
Hirata et al., Biol Pharm Bull 2010 : Tip associated protein (TAP), a key molecule in the nucleocytoplasmic transport of TNFalpha mRNA, was up-regulated by LPS , but this increase was impaired by the Tpl2 inhibitor
López-Pelaéz et al., Mol Biol Cell 2012 (Inflammation...) : The dissociation of the 4E-BP-eIF4E complex, a key event in the cap dependent mRNA translation initiation, is dramatically reduced in LPS stimulated Cot/tpl2-knockout ( KO ) macrophages versus LPS stimulated wild-type ( Wt ) macrophages
Roget et al., Mol Cell Biol 2012 : LPS stimulation of TPL-2 MEK-1/2 kinase activity requires TPL-2 release from p105