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Text-mined interactions from Literome

Tanaka et al., J Biol Chem 2000 : These results suggest that AGE, TNF-alpha , and E ( 2 ) can activate the RAGE gene through NF-kappaB and Sp-1, causing enhanced AGE-RAGE interactions, which would lead to an exacerbation of diabetic microvasculopathy
Mukherjee et al., Biochim Biophys Acta 2005 : TNFalpha , a proinflammatory cytokine, is a potent inducer of RAGE expression in endothelial cells ... The gp91phox subunit of NADPH oxidase appears to be the source of ROS that induces TNFalpha dependent mitochondrial ROS generation and subsequent RAGE expression
Fujita et al., Arterioscler Thromb Vasc Biol 2006 : Stimulation of human endothelial cells with candesartan as well as olmesartan decreased TNFalpha induced RAGE expression in both mRNA and protein levels along with the decrease in the activity of nuclear factor kappaB and the expression of inflammatory mediators such as vascular cell adhesion molecule (VCAM)-1
Bianchi et al., Neurobiol Aging 2010 (Encephalitis...) : We show here that : ( 1 ) S100B also stimulates AP-1 transcriptional activity in microglia via RAGE dependent activation of JNK ; ( 2 ) S100B upregulates IL-1beta and TNF-alpha expression in microglia via RAGE engagement ; and ( 3 ) S100B/RAGE induced upregulation of COX-2, IL-1beta and TNF-alpha expression requires the concurrent activation of NF-kappaB and AP-1
Zhang et al., Clin Sci (Lond) 2009 (Vascular Diseases) : AGEs ( advanced glycation end-products ) /RAGE ( receptor for AGEs ), LOX-1 [ lectin-like oxidized low-density lipoprotein receptor-1 ) and NF-kappaB ( nuclear factor kappaB ) signalling play key roles in TNF-alpha expression through an increase in circulating and/or local vascular TNF-alpha production
Wu et al., J Nutr Biochem 2011 : FBS incubated with MG and CA ( MG/CA-FBS ) evoked the greatest deleterious responses, as follows : ( 1 ) inducing proinflammatory tumor necrosis factor (TNF)-a and interleukin-1ß expression and ROS production in monocytic THP-1 cells, ( 2 ) stimulating TNF-a secretion in RAW 264.7 macrophages and ( 3 ) causing oxidative DNA damage and inducing the expression of receptor for AGEs (RAGE) , intercellular adhesion molecule-1 ( ICAM-1 ) and vascular cell adhesion molecule-1 in human umbilical vein endothelial cells
Piazza et al., Int J Immunopathol Pharmacol 2013 : Soluble RAGE ( sRAGE ) reduced S100B dependent secretion of TNF-alpha but did not decrease S100B dependent secretion of IL-6
Miyata et al., J Clin Invest 1996 (Amyloidosis...) : Induction of tumor necrosis factor-alpha (TNF) expression by MPs exposed to AGE-beta2M resulted from engagement of RAGE , as appearances of TNF transcripts and TNF antigen release into culture supernatants were prevented by addition of sRAGE, a process mediated, at least in part, by oxidant stress