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NFKB1 — RENBP

Text-mined interactions from Literome

Neumann et al., FEBS Lett 1999 : Hyaluronic acid with a molecular weight above 1.2 MDa ( HMW-HA ) inhibits the AGE induced activation of the transcription factor NF-kappaB and the NF-kappaB regulated cytokines interleukin-1alpha, interleukin-6 and tumor necrosis factor-alpha
Lal et al., Kidney Int 2002 : NF-kappaB was dose-dependently activated by AGE ... Antioxidants, vitamin E and nitecapone, prevented AGE dependent NF-kappaB activation and normalized PKC activity and associated TGF-beta1 transcription
Morcos et al., Diabetes 2002 (Diabetes Mellitus, Type 2...) : To further prove an AGE/CML induced NF-kappaB activation in pTECs, NF-kappaB activation was studied in cultured human pTECs by electrophoretic mobility shift assays ( EMSAs ) and Western blot ... The AGE- and CML dependent activation of NF-kappaBp65 and NF-kappaB dependent IL-6 expression could be inhibited using the soluble form of the receptor for AGEs (RAGE) ( soluble RAGE [ sRAGE ] ), RAGE-specific antibody, or the antioxidant thioctic acid ... The findings that excreted pTECs demonstrate activated NF-kappaB and IL-6 antigen and that AGE-albumin and CML lead to a perpetuated activation of NF-kappaB in vitro infer that a perpetuated increase in proinflammtory gene products, such as IL-6, plays a role in damaging the renal tubule
Zhang et al., Di Yi Jun Yi Da Xue Xue Bao 2003 : NF-kappa B could be activated by AGE-HSA in a time- and dose dependent manner, and the results obtained from immunochemical staining were consistent with those from EMSA
Seki et al., Metabolism 2003 (Arteriosclerosis) : To examine possible mechanisms for this effect, we studied nuclear factor-kappa B (NF-kappaB) activation and the tyrosine phosphorylation pathway ; AGE stimulated NF-kappaB activity, but phosphorylation of the platelet derived growth factor ( PDGF ) receptor was unchanged
Lu et al., Proc Natl Acad Sci U S A 2004 (Inflammation) : However, AGE stimulated NF-kappaB activity and mitogen activated protein kinase ( MAPK ) ( p44/42 ) phosphorylation were found markedly suppressed in R1-MC. Additionally, AGE stimulated macrophage chemotaxis protein 1 and RAGE overexpression were abolished in R1-MC
De Oliveira et al., J Lab Clin Med 2005 (Diabetes Mellitus, Type 2...) : In the presence of insulin ( 10-100 nmol/L ), the stimulation of NF-kappaB protein expression by AGE-BSA ( 100 microg/mL ) was decreased, whereas the expression of PPAR-gamma, protein was enhanced ... 15-Deoxyprostaglandin J2, a direct activator of PPAR-gamma, decreased AGE-BSA stimulated NF-kappaB expression
Zhao et al., Di Yi Jun Yi Da Xue Xue Bao 2005 : A fusion protein with a molecular weight of about 45 kD was purified, which could interact with anti-RAGE antibody and AGE and block AGE induced nuclear factor (NF)-kB activation in the endothelial cells
Harashima et al., Biochem J 2006 (Diabetes Mellitus, Experimental...) : A transfection experiment revealed that the mRNA was actually translated as deduced to yield the secretory protein working as a decoy in AGE induced NF-kappaB ( nuclear factor kappaB ) activation
Schiekofer et al., Exp Clin Endocrinol Diabetes 2006 (Diabetes Complications...) : Postprandial mononuclear NF-kappaB activation is independent of the AGE-content of a single meal ... Postprandial mononuclear NF-kappaB activation after a single meal is independent of the AGE-content of the ingested protein
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 )
San Martin et al., Free Radic Biol Med 2007 (Vascular Diseases) : AGE stimulated NF-kappaB activity was abolished by DPI and the superoxide scavenger MnTBAP
Sayed et al., Phytother Res 2007 : Thymoquinone decreases AGE induced NF-kappaB activation in proximal tubular epithelial cells ... A significant reduction of AGE induced NF-kappaB-activation and Il-6 expression was observed
Sun et al., Basic Res Cardiol 2009 : AGE-HSA also promoted EPCs apoptosis and inhibited EPCs migration and increased NF-kappaB activity, these effects could be significantly attenuated by the anti-RAGE neutralizing antibody as well as by p38 and ERK MAPK inhibitors
Deo et al., J Biochem Mol Toxicol 2009 : Stimulation of human microvascular endothelial cells with BSA-LMM-AGE-Cas complexes significantly increased mRNA expression of the receptor of AGE (RAGE), galectin-3 ( AGE-R3 ), tumor necrosis factor alpha, and a marker of the mitogen activated protein kinase pathway ( MAPK-1 ), as well as p65NF-kappaB activation
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
Ide et al., Microvasc Res 2010 (Diabetic Nephropathies) : PEDF or neutralizing antibody raised against RAGE ( receptor for AGE ) was found to inhibit the AGE induced oxidative stress generation and subsequent NF-kappaB activation in mesangial 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)