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GRAP2 — TLR2

Text-mined interactions from Literome

Hirao et al., Life Sci 2010 (Inflammation) : In TLR2 ligand stimulated HDPF, specific inhibitors of extracellular signal regulated kinase ( ERK ) 1/2, p38 , c-jun NH ( 2 ) -terminal kinase ( SAP/JNK ), NF-kappaB or catechins markedly reduced the level of pro-inflammatory mediators and the phosphorylation of these signal transduction molecules was suppressed by catechins
Beaudoin et al., Biochem Biophys Res Commun 2012 (Cystic Fibrosis) : Inactivation of mucA ( the gene responsible for the mucoid phenotype ) in PAO1 leads to p38a MAPK activation by both TLR2 and TLR5, as observed in the clinical mucoid isolate PACF508
Zhang et al., PloS one 2013 (MAP Kinase Signaling System) : YCP interaction with TLR2 and TLR4 led to the activation of intracellular p38 , ERK and JNK, as well as the translocation of transcriptional factor NF-?B into nucleus
Wagner et al., Arterioscler Thromb Vasc Biol 2013 (Ischemia...) : The effects of anti-TLR2 ABs were similar to those exerted by stromal cell derived factor-1, and we show that anti-TLR2 ABs yet not TLR2 ligands lead to comparable activation of extracellular signal regulated kinase1/2 and AKT but not p38 mitogen activated protein kinase as activation of the CXCR4 canonical signal transduction pathways by stromal cell derived factor-1