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PI3 — TLR4

Text-mined interactions from Literome

Li et al., Infect Immun 2003 : Further, these studies suggest that PI3-kinase is an important mediator of LPS and IL-1 beta signaling leading to NF-kappa B activation in endothelial cells and that Akt is necessary but not sufficient for NF-kappa B activation by TLR4
Guiducci et al., J Exp Med 2008 : Phosphatidylinositol-3 kinase (PI3K) has been shown to be activated by TLR triggering in multiple cell types ; however, its role in pDC function is not known
Watarai et al., Proc Natl Acad Sci U S A 2008 : However, when coupled with Sema6D, a ligand for Plexin-A1, limited TLR-stimulation resulted in PDC-TREM mediated DAP12 dependent phosphorylation of phosphoinositide 3-kinase (PI3K) and extracellular regulated kinase (Erk) 1/2 at 6-9 h, and IFN-alpha was produced
Zhang et al., J Neuroimmunol 2008 (Disease Models, Animal) : Here, we demonstrate an essential role for the TLR4 mediated phosphoinositide 3-kinase (PI3K)/Akt signaling
Zhang et al., Cell Biol Toxicol 2012 (Prostatic Neoplasms) : TLR4 ligation resulted in a marked increase in the phosphorylation of phosphatidylinositol 3-kinase (PI3-K) and Akt