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GRAP2 — TLR4

Text-mined interactions from Literome

Aki et al., Genes Cells 2005 : Furthermore, overall cellular tyrosine phosphorylation and TLR4 mediated activation of IkappaB-alpha, Erk and p38 but not of JNK, were also down-regulated in Csk knockdown cells
He et al., J Cell Biochem 2010 : The activation of TLR4 by LPS modulated the expression of TLRs, induced the phosphorylation of NF-kappaB, P38 , and ERK42/44, and up-regulated the gene expression of cytokines IL-8, IFN-alpha, IFN-beta, and TNF-alpha, suggesting EPCs expressed functional TLR4
Kim et al., Gastroenterology research and practice 2010 : TLR4 , expressed in insulin target tissues, activates proinflammatory kinases JNK, IKK, and p38 that impair insulin signal transduction directly through inhibitory phosphorylation of insulin receptor substrate (IRS) on serine residues
Tsai et al., PloS one 2011 : These results strongly suggest that Der-p2 is capable of triggering B cell activation and MKP-1 activated p38/MAPK dephosphorylation regulated TLR4 induction, which subsequently enhances host immune, defense responses and development of effective allergic disease therapeutics in B cells
Zbinden-Foncea et al., Cell Biol Int 2012 : TLR2 and TLR4 activation induces p38 MAPK dependent phosphorylation of S6 kinase 1 in C2C12 myotubes
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
Yang et al., Lab Invest 2013 (Acute Lung Injury...) : Inhibition of TLR4 expression in the lung tissue by infection with pGCSIL-GFP-lentivirus expressing small hairpin RNAs targeting the TLR4 gene ( TLR4-shRNA lentivirus ) significantly attenuated ALI, lung inflammation, and activity of p38MAPK and AP-1 in the lung tissue