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HSPG2 — IRF6

Text-mined interactions from Literome

Zhang et al., Int Immunopharmacol 2001 : Phosphatidic acid was reduced to basal level by butanol after LPS stimulation for 2.5 min and by butanol plus D609 after LPS stimulation for 2.5 or 10 min. Taken together, these data indicate that activation of RAW264.7 cells by LPS can be mediated by the activities of both PC-PLC and PC-PLD
Hiller et al., Cell Signal 2002 : In contrast to zymosan and bacteria, PLC-gamma 2 was not phosphorylated by stimulation with lipopolysaccharide (LPS) , phorbol ester or calcium ionophore
Coffey et al., Immunology 1992 : FMLP but not LPS stimulated phospholipase C (PLC) , determined by the release of [ 3H ] inositol phosphates
Ramana et al., J Biol Chem 2006 : The AR inhibition or ablation significantly attenuated LPS induced activation of protein kinase C ( PKC ) and phospholipase C (PLC) , nuclear translocation of NF-kappaB, and phosphorylation and proteolytic degradation of IkappaBalpha in macrophages
Chow et al., New Horiz 1995 : Activation of PLC by LPS results in the release of diacylglycerol and inositol 1,4,5-trisphosphate
Lütjohann et al., Toxicol Lett 1998 : LPS and quartz dust induced a short-term increase of PLC cleavage products
Chen et al., J Immunol 1998 : These data suggest that LPS activates PI-PLC and PC-PLC via an upstream tyrosine kinase to induce PKC activation, resulting in the stimulation of NF-kappaB DNA-protein binding, then initiated the expression of iNOS and NO release