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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