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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