Gene interactions and pathways from curated databases and text-mining

◀ Back to IL8

IL8 — PTK7

Text-mined interactions from Literome

Li et al., Infect Immun 1999 : Further studies with the L5F11 cell line showed that IL-8 gene transcription induced by H. pylori was blocked by the protein tyrosine kinase inhibitor herbimycin A but not by the protein kinase C inhibitor calphostin C or by the protein kinase G inhibitor KT5823
Xiao et al., Clin Exp Immunol 2001 : C1q bearing immune complexes induce IL-8 secretion in human umbilical vein endothelial cells ( HUVEC ) through protein tyrosine kinase- and mitogen activated protein kinase dependent mechanisms : evidence that the 126 kD phagocytic C1q receptor mediates immune complex activation of HUVEC ... These experiments demonstrate that C1q-IC induced production of IL-8 in HUVEC is dependent upon the activation of PTK and MAPK
Bian et al., Exp Eye Res 2003 (Translocation, Genetic) : These results suggest that activation of DEX-sensitive, CSA-resistant MEK/ERK and p38 pathways, and activation of NF-kappaB, PKC, and PTK are essential for IL-8 and MCP-1 expression by hRPE cells
Øvrevik et al., Toxicological sciences : an official journal of the Society of Toxicology 2004 : The IL-8 induction was significantly attenuated by inhibitors of the mitogen activated protein kinases ( MAPKs ), p38 ( SB202190 ) and extracellular signal regulated kinase ( ERK ) -1 and -2 ( PD98059 ), as well as a general protein tyrosine kinase ( PTK ) inhibitor ( genistein )
Zeng et al., Acta Pharmacol Sin 2005 : Inhibitors of PKC ( calphostin C, 50-500 nmol/L and RO-31-8220, 10-100 nmol/L ), CaM ( W7, 28-280 micromol/L ), ERK1/2 MAPK ( PD 98059, 2-20 micromol/L ), p38 MAPK ( SB 203580, 0.6-6 micromol/L ), JNK MAPK ( curcumin, 2-10 micromol/L ), and NF-kappaB ( PDTC, 10-100 nmol/L ) markedly reduced Hcy 100 micromol/L induced production of MCP-1 and IL-8 in human cultured whole blood, but the inhibitors of PTK ( genistein, 2.6-26 micromol/L and tyrphostin, 0.5-5 micromol/L ) had no obvious effect on MCP-1 and IL-8 production
Wawszczyk et al., Acta Pol Pharm 2013 : Role of protein tyrosine kinase in the effect of IP6 on IL-8 secretion in intestinal epithelial cells ... The aim of this study was to determine the role of protein tyrosine kinase ( PTK ) in secretion of IL-8 , a central proinflammatory cytokine, by unstimulated and IL-1beta stimulated intestinal epithelial cells Caco-2 treated with IP6 ( 1 and 2.5 mM )
Gross et al., Gastroenterology 1995 : The aim of this study was to improve the understanding of the regulation of IL-8 synthesis by investigating the roles of protein kinase C ( PKC ), protein kinase A (PKA), and protein tyrosine kinase ( PTK ) in the induction of IL-8 ... However, induction of IL-8 by IL-1 beta or TNF-alpha was reduced by the PTK inhibitors herbimycin ( by 79 % or 89 %, respectively ) and genistein ( by > 95 % )
Chaudhary et al., J Biol Chem 1996 : 1- ( 5-Isoquinolinesulfonyl ) -2-methylpiperazine, HCl ( 50 microM ) and staurosporine ( 1 microM ), potent inhibitors of protein kinase C, and genistein ( 100 microM ), a specific protein tyrosine kinase inhibitor blocked IL-1beta induced IL-8 gene expression
Beales et al., Cytokine 1997 : The aim of this study was to investigate the roles of protein kinase A (PKA), protein kinase C ( PKC ), protein tyrosine kinase ( PTK ) and intracellular calcium in the induction of IL-8 production by gastric epithelial cells
Ding et al., Biochem Biophys Res Commun 1997 : Geldanamycin, a more potent PTK inhibitor, at doses of 0.5, 1, and 2 microM dose-dependently reduced HP toxin induced endothelial cell IL-8 expression by 24.8, 26, and 44.3 % respectively ... It is concluded that HP and its toxin can increase IL-8 expression in endothelial cells, and the expression of IL-8 elicited by HP toxin, TNF-alpha, and LPS is partially dependent on PTK but not PKA or PKC activation