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AKT3 — IL8

Text-mined interactions from Literome

Osawa et al., Infect Immun 2002 : IL-8 expression by TNF-alpha was inhibited when two survival signals, nuclear factor kappaB (NF-kappaB) and phosphatidylinositol 3-kinase (PI3K)/Akt, were inhibited by a mutant form of inhibitor of NF-kappaB ( IkappaB ) ; by dominant negative ( kinase-dead ) Akt ; or by treatment with LY 294002, an inhibitor of PI3K
Grzesiak et al., Int J Cancer 2005 (Adenocarcinoma...) : These results implicate GSK3 and PKB/Akt in the integrin mediated regulation of PTHrP, IL-6 and IL-8 in pancreatic cancer
Newcomb et al., J Biol Chem 2005 : Inhibition of PI 3-kinase and Akt attenuated RV39 induced NF-kappaB transactivation and IL-8 expression
Kobashi et al., Circ Res 2005 (Atherosclerosis) : The inhibitory effect of adiponectin on TNF-alpha induced IL-8 synthesis was abrogated in part by pretreatment with the PI3 kinase inhibitor LY294002 or by Akt siRNA transfection, suggesting that Akt activation might inhibit IL-8 synthesis induced by TNF-alpha
Brkovic et al., J Leukoc Biol 2007 : Finally, both angiopoietins showed a synergistic effect on the induction of Akt phosphorylation mediated by CXCL8/IL-8
Xu et al., Rheumatology (Oxford) 2007 (Arthritis, Rheumatoid) : TNF-alpha induced production of IL-1beta, IL-6 and IL-8 was hampered by treatment with the phosphatidylinositol 3 (PI3) kinase inhibitor LY294002, suggesting that inhibition of Akt activation might inhibit IL-1beta, IL-6 and IL-8 production induced by TNF-alpha
MacManus et al., Mol Cancer Res 2007 (Prostatic Neoplasms) : Immunoblotting using phospho-specific antibodies confirmed that recombinant human IL-8 induced rapid time dependent phosphorylation of Akt and the mammalian target of rapamycin substrate proteins, 4E-BP1 and ribosomal S6 kinase, resulting in a downstream phosphorylation of the ribosomal S6 protein ( rS6 )
Zhao et al., Biochem Pharmacol 2008 : The pharmacological inhibitor of phosphatidylinositol 3-kinase (PI3K) ( wortmannin ) and dominant negative forms of p85 ( the regulatory subunit of PI3K ) or Akt enhance, while constitutive active forms of p110 ( the catalytic subunit of PI3K ) or Akt inhibit , NF-kappaB activation and the target gene interleukin (IL)-8 induced by MDP
Venkatachalam et al., Am J Physiol Heart Circ Physiol 2008 (Hyperglycemia) : Resveratrol inhibits high glucose induced PI3K/Akt/ERK dependent interleukin-17 expression in primary mouse cardiac fibroblasts
Kobashi et al., Journal of inflammation (London, England) 2009 : Furthermore, we examined the effect of IL-8 on the phosphorylation of Akt induced by insulin
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
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
Tabassam et al., Helicobacter 2012 (Helicobacter Infections) : Akt , FoxO1, or FoxO3a siRNA reduced H. pylori induced interleukin-8 production
He et al., Cancer Chemother Pharmacol 2013 (Carcinoma, Non-Small-Cell Lung...) : EGCG inhibited HPV-16 oncoprotein induced angiogenesis conferred by NSCLC through the inhibition of HIF-1a protein expression and HIF-1a dependent expression of VEGF, IL-8 , and CD31 as well as activation of Akt , suggesting that HIF-1a may be a potential target of EGCG against HPV related NSCLC angiogenesis