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IKBKG — PTGS2

Text-mined interactions from Literome

Nakatani et al., Mol Pharmacol 2004 (Brain Neoplasms...) : These results suggest that gamma-mangostin directly inhibits IKK activity and thereby prevents COX-2 gene transcription, an NF-kappaB target gene, probably to decrease the inflammatory agent stimulated PGE ( 2 ) production in vivo, and is a new useful lead compound for anti-inflammatory drug development
Kundu et al., Carcinogenesis 2006 : Topical application of Bay 11-7082 also abrogated TPA induced NF-kappaB activation and COX-2 expression, supporting the involvement of IKK in TPA induced COX-2 expression
Pan et al., Biochem Pharmacol 2006 (Cocarcinogenesis...) : Taken together, these results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation associated tumorigenesis
Hwang et al., Carcinogenesis 2007 : Taken together, 9Z,11E-CLA inhibits NF-kappaB driven-COX-2 expression by blocking the IKK and PI3K-Akt signaling in TPA treated hairless mouse skin in vivo, which may account for its previously reported anti-tumor promoting effects
Polk et al., Am J Physiol Cell Physiol 2007 (Nephritis) : RhoA regulation of NF-kappaB activation is mediated by COX-2 dependent feedback inhibition of IKK in kidney epithelial cells
Pan et al., J Agric Food Chem 2008 : Taken together, these results show that pterostilbene down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NFkappaB by interfering with the activation of PI3K/Akt/IKK and MAPK
Zhang et al., Inflammation 2010 (Inflammation) : These results suggest that resistin enhances COX-2 expression in mouse macrophage cells in a TAK1-IKK-NF-kappaB dependent manner and therefore plays a critical role in inflammatory processes
Kumar et al., Carcinogenesis 2012 (Carcinoma, Squamous Cell...) : Single application of NX ( 1.0mg/mouse ) prior to 12-O-tetradecanoylphorbol 13-acetate ( TPA ) application significantly inhibited TPA induced skin edema, hyperplasia, thymidine incorporation and ornithine decarboxylase (ODC) activity ; expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) ; phosphorylation of extracellular signal regulated kinases ( ERK ) 1/2, p38 and c-jun N-terminal kinase ( JNK ) mitogen activated protein kinases ( MAPKs ) ; and activation of I kappa B kinase (IKK) , I?Ba and nuclear factor-kappa B ( NF-?B ) in mouse skin