Gene interactions and pathways from curated databases and text-mining

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CAV1 — IRF6

Text-mined interactions from Literome

Lei et al., Infect Immun 2000 : In RAW264.7 cells, both caveolin-1 mRNA and protein levels are down-regulated by LPS ... In TG-elicited C3HeB/FeJ peritoneal macrophages, in contrast, expression of both caveolin-1 protein and mRNA is up-regulated in vitro in response to LPS stimulation
Walton et al., Arterioscler Thromb Vasc Biol 2003 : Supporting an important role for caveolae in LPS action, overexpression of caveolin-1 enhanced LPS induced IL-8 synthesis
Lei et al., Infect Immun 2005 : Interestingly, polymyxin B ( 5 microg/ml ) and RsDPLA show only a limited capacity to inhibit LPS induced caveolin-1 expression ... These findings suggest that expression of caveolin-1 in response to LPS may only partially be dependent upon lipid A. Recombinant tumor necrosis factor alpha marginally induces caveolin-1, suggesting that the ability of LPS to regulate caveolin-1 is not mediated primarily through an autocrine/paracrine mechanism involving this cytokine ... Gamma interferon treatment inhibits the induction of caveolin-1 by LPS in macrophages
Kamoun et al., Hepatology 2006 : Antagonizing ET-1 effects and blocking its activation in LPS pretreated SECs decreased the LPS induced overexpression of CAV-1 as well as the inhibition of ET-1 induced NOS activity
Tiruppathi et al., J Biol Chem 2008 : Knockdown of NF-kappaB subunit p65/RelA expression with small interfering RNA also prevented LPS induced Cav-1 expression ... Thus, LPS mediates NF-kappaB dependent Cav-1 expression that results in increased caveolae number and thereby contributes to the mechanism of increased transendothelial albumin permeability
Kwok et al., Shock 2010 : In this report, liver sinusoidal endothelial cells ( LSECs ) from wild-type ( WT ) and Cav-1 knockout ( KO ) mice were isolated, pretreated with 100 ng/mL LPS for 6 h, and treated with 10 nmol ET-1 for 30 min. Data showed that LPS increased Cav-1 protein expression ( +88 % ; P < 0.05 ) and inhibited ET-1 mediated eNOS activation and NO production in WT LSECs
Kwok et al., Am J Physiol Gastrointest Liver Physiol 2009 : A dose ( 0.25 microg/ml ) of filipin for 30 min produced a similar effect ( +111 %, P < 0.05 ). CD induced the perinuclear localization of Cav-1 and eNOS and stimulated NO production in the same region. Readdition of 0.5 mM cholesterol to saturate CD reversed these effects. Both the combined treatment with CD and ET-1 ( CD + ET-1 ) and with filipin and ET-1 stimulated eNOS activity ; however, pretreatment with endotoxin ( LPS ) abrogated these effects. Following LPS pretreatment, CD + ET-1 failed to stimulate eNOS activity ( +51 %, P > 0.05 ), which contributed to the reduced levels of eNOS-Ser1177 phosphorylation and eNOS-Thr495 dephosphorylation, the LPS/CD induced overexpression and translocation of Cav-1 in the perinuclear region, and the increased perinuclear colocalization of eNOS with Cav-1