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Text-mined interactions from Literome

Huttunen et al., J Biol Chem 1999 (Neuroblastoma) : Both the RAGE mediated neurite outgrowth and activation of NF-kappaB are blocked by deletion of the cytoplasmic domain of RAGE
Yan et al., Restor Neurol Neurosci 1998 : Abeta-RAGE interaction also activated NF-kappaB , resulting in neuronal up-regulation of macrophage-colony stimulating factor ( M-CSF ) which also induced microglial migration
Hsieh et al., Biochem Biophys Res Commun 2004 : We show here that NF-kappaB which is a downstream regulator in RAGE mediated transduction pathways can be activated by addition of extracellular S100 proteins, and translocation of S100 proteins was inhibited by soluble RAGE
Isermann et al., Herz 2004 (Atherosclerosis...) : The ligand-RAGE-interaction results in an activation of NF-kappaB , increased expression of cytokines, chemokines, and adhesion molecules and induces oxidative stress
Marx et al., Diabetes 2004 : These effects on RAGE expression were caused by an inhibition of nuclear factor-kappaB (NF-kappaB) activation at the proximal NF-kappaB site of the RAGE promoter
Dumitriu et al., J Immunol 2005 : HMGB1/RAGE interaction results in downstream activation of MAPKs and NF-kappaB
Loeser et al., Arthritis Rheum 2005 (Osteoarthritis) : Stimulation of RAGE signaling can lead to MAP kinase activation and increased NF-kappaB activity
Hein et al., Clin Chim Acta 2006 (Bone Resorption...) : The AGE-RAGE interaction additionally induces activation of nuclear factor kB (NF-kB) in RAGE bearing cells ( e.g., cells participating in bone turnover )
Andrassy et al., Am J Pathol 2006 (Disease Models, Animal...) : Inflamed gut biopsy tissue demonstrated a significant up-regulation of RAGE and increased NF-kappaB activation
Yamagishi et al., Ophthalmic Res 2007 (Diabetes Mellitus, Experimental...) : These results demonstrated that PEDF could inhibit diabetes- or AGE induced RAGE gene expression by blocking the superoxide mediated NF-kappaB activation
Yamagishi et al., Microvasc Res 2008 (Diabetic Retinopathy...) : Since the crosstalk between the AGEs-RAGE and the renin-angiotensin system has also been proposed in the pathogenesis of PDR, we investigated here whether olmesartan, an angiotensin II type 1 receptor blocker, inhibited the AGEs elicited angiogenesis in vitro by suppressing the NF-kappaB mediated RAGE expression
Bengmark et al., JPEN J Parenter Enteral Nutr 2007 (Diabetes Mellitus...) : RAGE , a member of the immunoglobulin superfamily of cell surface molecules and receptor for advanced glycation end products, known since 1992, functions as a master switch, induces sustained activation of nuclear factor kappaB (NFkappaB) , suppresses a series of endogenous autoregulatory functions, and converts long lasting proinflammatory signals into sustained cellular dysfunction and disease
Wang et al., J Neurosci Res 2008 : RAGE knockdown inhibited retinoic acid induced activation and blocked nuclear translocation of NF-kappaB, suggesting RAGE regulates activation of NF-kappaB
Ghavami et al., J Leukoc Biol 2008 (MAP Kinase Signaling System) : Our data indicate that S100A8/A9 promoted cell growth occurs through RAGE signaling and activation of NF-kappaB
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
Pietkiewicz et al., Postepy Hig Med Dosw 2008 (Atherosclerosis...) : Engagement of RAGE in intracellular signaling leads to the activation of the proinflammatory transcription factor NF-kappaB to sustained cellular dysfunction and tissue destruction
Xia et al., International journal of molecular sciences 2008 : Silencing RAGE expression by specific siRNA effectively suppressed NF-kappaB activity, hepatic stellate cell activation, and accumulation of extracellular matrix proteins in the fibrotic liver, and also greatly improved the histopathology and the ultrastructure of liver cells
Chuong et al., J Cell Physiol 2009 : The aim of this study was to investigate the inhibitory effect of the soluble-RAGE ( sRAGE ), the extracellular domain of RAGE, on RAGE expression and NF-kappaB translocation in human-salivary gland-cell-lines ( HSG )
Farmer et al., Pharmacol Ther 2009 (Disease Models, Animal...) : RAGE is upregulated as a consequence of activation of the ubiquitous pro-inflammatory transcription factor NF-kappaB which is activated in response to diverse inflammatory stimuli including hyperglycaemia, oxidised low density lipoprotein ( oxLDL ) and reduced shear stress ... RAGE binding by circulating advanced glycation endproducts ( AGEs ) or S100 protein released by activated leukocytes results in the generation of reactive oxygen species ( ROS ) and further activation of NF-kappaB
Qin et al., J Immunol 2009 (Arthritis, Experimental) : These results demonstrate that HMGB1 enhances the proinflammatory activity of LPS by promoting the phosphorylation of MAPK p38 and by the activation of NF-kappaB through RAGE
Hilmenyuk et al., Immunology 2010 (Food Hypersensitivity) : Finally, expression of the receptor for advanced glycation endproducts ( RAGE ) and activation of the transcription factor nuclear factor (NF)-kappaB by AGE were investigated ... AGE-OVA exposed immature DCs showed a stronger expression of RAGE and activation of the transcription factor NF-kappaB compared with OVA loaded immature DCs
You et al., Mol Cell Endocrinol 2010 : These findings suggest that PLC/CAMK IV-NF-kappaB is involved in RAGE mediated signaling pathway in human endothelial cells
Kim et al., Age (Dordrecht, Netherlands) 2010 : It is also known that AGE enhance the generation of RS and that the binding of AGE to a specific AGE receptor ( RAGE ) induces the activation of the redox-sensitive, pro-inflammatory transcription factor, nuclear factor-kappa B (NF-kB)
Grotterød et al., BMC cancer 2010 (Osteosarcoma) : S100A4 induced NF-kappaB activation was independent of the putative S100 protein receptor RAGE and the Ser/Thr kinases MEKK1, NIK and AKT
van Zoelen et al., Front Biosci (Schol Ed) 2011 (Communicable Diseases...) : Engagement of RAGE by its diverse ligands results in receptor dependent signaling and activation of NF-kappaB
de Bittencourt Pasquali et al., Cell Signal 2013 (Lung Neoplasms) : Besides, we observed that NF-kB acted as a downstream effector of p38 in RAGE downregulation by retinol, as NF-kB inhibition by SN50 ( 100µg/mL ) and siRNA to p65 blocked the effect of retinol on RAGE , and p38 inhibitors reversed NF-kB activation
Wautier et al., Proc Natl Acad Sci U S A 1994 (Diabetes Complications...) : Binding of diabetic erythrocytes to endothelium generated an oxidant stress, as measured by production of thiobarbituric acid-reactive substances ( TBARS ) and activation of the transcription factor NF-kappa B , both of which were blocked by probucol or anti-RAGE IgG
Bierhaus et al., Circulation 1997 : Binding of advanced glycation end products ( AGEs ) to the cellular surface receptor ( RAGE ) induces translocation of the transcription factor NF-kappaB into the nucleus and NF-kappaB mediated gene expression ... Electrophoretic mobility shift assays and Western blot analysis demonstrated that the AGE albumin induced translocation of NF-kappaB from the cytoplasm into the nucleus was suppressed in the presence of antisense RAGE but not by sense RAGE