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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to IL8

IL8 — PI3

Text-mined interactions from Literome

Schulte et al., FASEB J 2000 : Invasin triggered IL-8 production does not depend on invasin triggered uptake of bacteria, and is independent of a functional PI3-kinase
Al-Okla et al., Cell Microbiol 1999 : However, PI-3K activation is not involved in IL-8 release
Henriksen et al., J Immunol 2004 (Arteriosclerosis) : Elafin and murine SLPI also reduced endothelial IL-8 release in response to oxidized low density lipoprotein, LPS, and TNF-alpha and macrophage TNF-alpha production in response to LPS
Cowburn et al., Eur J Immunol 2004 : Inhibition of I kappa B-alpha phosphorylation, PI3-kinase or ERK1/2 activation blocked IL-8 release by both cytokines
Newcomb et al., J Biol Chem 2005 : We examined the role of phosphatidylinositol (PI) 3-kinase in RV-induced interleukin (IL)-8 expression ... Inhibition of PI 3-kinase and Akt attenuated RV39 induced NF-kappaB transactivation and IL-8 expression
Wrann et al., J Immunol 2007 (Sepsis) : In addition, PI3K inhibition resulted in strongly elevated TLR-4 mediated generation of IL-1beta and IL-8 in neutrophils when these cells were co-stimulated with C5a
Syeda et al., J Cell Physiol 2008 (MAP Kinase Signaling System) : The HNP induced IL-8 production was blocked by the Src tyrosine kinase inhibitor PP2, MEK1/2 inhibitor U0126, and the phosphatidylinositol 3 kinase (PI3K) inhibitor LY294002, but not by the JNK inhibitor SP600125 in both cell types
Tanaka et al., Biochem Biophys Res Commun 2008 : The PAR2 triggered IL-8 release was suppressed by inhibitors of MEK ( U0126 ) or PI3-kinase ( LY294002 ), and PAR2 stimulation indeed activated the downstream kinases, ERK and Akt
Yang et al., Microvasc Res 2009 (AIDS Dementia Complex) : Inhibitors of STAT1, mitogen activated protein kinase kinase ( MEK ) ( PD98059 ), and phosphatidyl inositol 3 kinase (PI3K) ( LY294002 ), blocked gp120 induced STAT1 activation and significantly diminished IL-8- , IL-6-, and gp120 induced monocyte adhesion and migration across in vitro BBB models
He et al., Rheumatol Int 2011 (Arthritis, Rheumatoid) : TNFa- or hypoxia induced secretion of VEGF and IL-8 and expression of HIF-1a were hampered by treatment with the PI3 kinase inhibitor LY294002, suggesting that inhibition of PI3 kinase/Akt activation might inhibit VEGF and IL-8 secretion and HIF-1a expression induced by TNFa or hypoxia
Ivison et al., Mediators Inflamm 2010 (Inflammation) : Release of the chemokine IL-8 in response to flagellin involves NF-?B, p38 MAP kinase, and phosphatidylinositol 3-kinase (PI3K)
Lin et al., J Biol Chem 2011 : In this study, we further investigated the roles of Rac1, phosphoinositide 3-kinase (PI3K) , and Akt in thrombin induced NF-?B activation and IL-8/CXCL8 expression
Zhang et al., J Cell Physiol 2012 (Carcinoma, Non-Small-Cell Lung...) : EGF stimulated IL-8 production, phosphorylation of Akt and Erk, and cell proliferation and movement could be inhibited by EGFR inhibitor ( Erlotinib ), PI3K inhibitor ( GDC-0941 BEZ-235 and SHBM1009 ), and ERK1/2 inhibitor ( PD98059 )
Britschgi et al., Cancer Cell 2012 (Breast Neoplasms...) : Mechanistically, PI3K/mTOR inhibition increased IRS1 dependent activation of JAK2/STAT5 and secretion of IL-8 in several cell lines and primary breast tumors