Gene interactions and pathways from curated databases and text-mining

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APOA1 — TNF

Text-mined interactions from Literome

Hyka et al., Blood 2001 (Acute-Phase Reaction...) : Apolipoprotein A-I inhibits the production of interleukin-1beta and tumor necrosis factor-alpha by blocking contact mediated activation of monocytes by T lymphocytes
Imai et al., Surg Today 2003 (Endotoxemia) : ApoA-I inhibited the release of serum TNF-Alpha and improved the survival rates of rats with endotoxemia
Beers et al., Biochemistry 2006 : To determine the molecular mechanisms responsible for the effect of TNF alpha on the apoAI promoter activity, HepG2 cells were exposed to both genetic and pharmacological modulators of TNF alpha mediated signaling in the presence or absence of TNF alpha ... Treatment with SB202190 ( p38 MAP kinase inhibitor ) alone significantly increased apoAI promoter activity ; however, in the presence of TNF alpha , apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190 ... These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation
Yan et al., Life Sci 2006 (Endotoxemia...) : To investigate the mechanisms, we measured tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) levels in the serum and bronchoalveolar lavage (BAL) fluid and found that ApoA-I could significantly inhibit LPS induced increases in the IL-1beta and TNF-alpha levels in serum ( P < 0.05, respectively ), as well as in the IL-1beta, TNF-alpha, and IL-6 levels in BAL fluid ( P < 0.01 and P < 0.05, P < 0.05, respectively )
Jiao et al., Cytokine 2008 (Respiratory Distress Syndrome, Adult...) : We found that ApoA-I could attenuate LTA induced acute lung injury and inflammation and significantly inhibit LTA induced IL-1beta and TNF-alpha accumulation in the serum ( P < 0.01 and P < 0.05, respectively ), as well as in bronchoalveolar lavage (BAL) fluid ( P < 0.01 and P < 0.05, respectively )
Mogilenko et al., Biochemistry 2009 : Role of the nuclear receptors HNF4 alpha, PPAR alpha, and LXRs in the TNF alpha mediated inhibition of human apolipoprotein A-I gene expression in HepG2 cells ... In this work, we have demonstrated that treatment of HepG2 human hepatoma cells with chemical inhibitors for JNK, p38 protein kinases, and NFkappaB transcription factor abolishes the TNFalpha mediated inhibition of human apoA-I gene expression in HepG2 cells ... Treatment of HepG2 cells with PPARalpha antagonist ( MK886 ) or LXR agonist ( TO901317 ) abolishes the TNFalpha mediated decrease in the level of apoA-I gene expression ... PPARalpha agonist ( WY-14643 ) abolishes the negative effect of TNFalpha on apoA-I gene expression in the case of simultaneous inhibition of MEK1/2, although neither inhibition of MEK1/2 nor addition of WY-14643 leads to the blocking of the TNFalpha mediated decrease in the level of apoA-I gene expression individually ... These results suggest that nuclear receptors HNF4alpha, PPARalpha, and LXRs are involved in the TNFalpha mediated downregulation of human apoA-I gene expression and apoA-I protein secretion in HepG2 cells
Orlov et al., Biochem Biophys Res Commun 2010 : Stimulation of HepG2 cells by TNFalpha leads to activation of the distal alternative apoA-I promoter and downregulation of the proximal alternative and the canonical apoA-I promoters
Mogilenko et al., FASEB J 2012 : We have shown that endogenous ApoA-I stabilizes ABCA1, moreover, down-regulation of ApoA-I by siRNA results in an increase of Toll-like receptor 4 (TLR4) mRNA and membrane surface protein expression, as well as an enhancement of bacterial lipopolysaccharide (LPS) induced expression of tumor necrosis factor-a (TNF-a) , interleukin 1ß (IL-1ß), and inducible nitric oxide synthase ( NOS2 ) genes in human macrophages ... Obtained results suggest that endogenous ApoA-I has anti-inflammatory properties, presumably due to ABCA1 stabilization in macrophages ; these results elucidate the cell type-specific mechanism of the TNF-a mediated regulation of apoA-I gene expression in monocytes and macrophages
Ramírez Alvarado et al., Nutr Hosp 2012 (Insulin Resistance...) : In human hepatocytes, TNF-a inhibits expression of APO AI , which may decrease the secretion of high density lipoproteins
Hardardóttir et al., Lymphokine Cytokine Res 1994 (Inflammation) : TNF or IL-1 did not affect hepatic apo E or apo A-I mRNA levels while a combination of TNF + IL-1 decreased both mRNA levels by 50 %
Mehran et al., Am J Physiol 1995 : De novo synthesis of apo A-I , apo B-100, and apo B-48 was also markedly reduced by TNF-alpha
Song et al., Cytokine 1998 : IL-1 beta and TNF-alpha suppress apolipoprotein ( apo ) E secretion and apo A-I expression in HepG2 cells ... The present results suggest that IL-1 beta and TNF-alpha suppress hepatic apo A-I expression and secretion but not expression of apo E, which could contribute to the abnormal lipid metabolism in certain cytokine mediated inflammatory diseases
Ramharack et al., Arterioscler Thromb Vasc Biol 1998 : Dominant negative effect of TGF-beta1 and TNF-alpha on basal and IL-6 induced lipoprotein ( a ) and apolipoprotein ( a ) mRNA expression in primary monkey hepatocyte cultures