Gene interactions and pathways from curated databases and text-mining

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RENBP — TNF

Text-mined interactions from Literome

Matsuo et al., Kidney Int 2000 (Amyloidosis...) : AGE-beta2m induced significant TNF-alpha and IL-1Ra production by macrophage ... The addition of exogenous TGF-beta1 ( 0.1 to 10 ng/mL ) decreased AGE-beta2m induced TNF-alpha production and increased IL-1Ra production in a dose dependent fashion
Zheng et al., Mol Med 2001 (Diabetes Mellitus, Type 1...) : B ) LZ stimulated the uptake and degradation of ( 125 ) I-labeled AGE-BSA and ( 25 ) I-human serum AGE by Mf, while suppressing AGE induced TNFalpha and IGF-I production
Meiners et al., J Neural Transm 2004 : Furthermore, the effects of four xanthine derivatives on AGE induced TNF-alpha release were investigated ... The xanthine derivatives pentoxyphylline and propentophylline attenuate AGE induced TNF-alpha release in a dose dependent manner ... The inhibition of the AGE induced TNF-alpha release by pentoxyphylline and propentophylline provides interesting pharmacological strategies for diseases with local neuroinflammation such as Alzheimer 's disease
Reznikov et al., Clin Nephrol 2004 : However, in the presence of 1 or 10 ng/ml of endotoxin, AGE augmented the production of IL-1 and TNF above that induced by endotoxin alone
Rashid et al., Isr Med Assoc J 2006 : Both AGE modified beta2m and AGE-HSA significantly increased TNF-alpha and IL-1beta secretion by human PMO in a dose dependent manner ( 50-200 microg/ml )
Nah et al., FEBS Lett 2007 (Osteoarthritis) : The stimulatory effect of AGE-BSA on MMP-1, -3, and -13 were reversed by treatment with specific JNK, p38 inhibitors, suggesting JNK and p38 are involved in AGE-BSA induced MMPs and TNF-alpha ... We also observed that NF-kappaB is involved in AGE-BSA induced TNF-alpha ... Pretreatment with soluble receptor for AGE ( sRAGE ) also reduced AGE stimulated MMPs and TNF-alpha , implicating the involvement of receptor for AGE (RAGE)
Hasegawa et al., Kidney Int 1991 (Albuminuria...) : These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from M phi
Berbaum et al., Cytokine 2008 : Our study showed that monocyte chemoattractant protein-1 ( MCP-1 ) and tumor necrosis factor ( TNF-alpha ) were both released in a time dependent manner from both RAW 264.7 macrophages and N-11 microglia upon stimulation with BSA-AGE or lipopolysaccharide (LPS), which was used as a positive control
Rasheed et al., Arthritis Res Ther 2009 : In the present study, we examined the effect of epigallocatechin-3-gallate ( EGCG ) on AGE-modified-BSA (AGE-BSA) induced activation and production of TNFalpha and MMP-13 in human OA chondrocytes ... EGCG significantly decreased AGE stimulated gene expression and production of TNFalpha and MMP-13 in human chondrocytes ... The inhibitory effect of EGCG on the AGE-BSA induced expression of TNFalpha and MMP-13 was mediated at least in part via suppression of p38-MAPK and JNK activation
Takahashi et al., Eur J Pharmacol 2010 : In a previous study, we found that glyceraldehyde derived AGE ( AGE-2 ) and glycolaldehyde derived AGE ( AGE-3 ) at 100 microg/ml induced the expressions of ICAM-1 and CD40 on monocytes and the production of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha in human peripheral blood mononuclear cells
Chandler et al., Mol Nutr Food Res 2010 (Alzheimer Disease) : This study tested the pure compounds apigenin and diosmetin as well as extracts from silymarin, uva ursi ( bearberry ) and green olive leaf for their ability to attenuate AGE induced NO and TNF-alpha production
Liang et al., Diabetes Metab Res Rev 2010 : AGE significantly increased tumour necrosis factor-alpha (TNF-alpha) , a major pro-inflammatory cytokine
Mori et al., Br J Pharmacol 2010 : In addition, CIP inhibited AGE-2- and AGE-3 induced expressions of ICAM-1, B7.1, B7.2 and CD40 in monocytes, the production of TNF-alpha and IFN-gamma and lymphocyte proliferation in PBMC
Qin et al., International journal of molecular sciences 2012 : The treatment of macrophages with AME effectively inhibited AGE induced IL-1ß and TNF-a secretion and mRNA expression in macrophages
Morita et al., J Diabetes Complications 2013 : Antioxidant TEMPOL almost completely inhibited AGE3 induced TNF-a secretion, whereas NF-?B inhibitor PDTC partly suppressed AGE3 induced 8-OHdG production
Yang et al., Pharmacology 2013 : In the present study, we examined the effect of curcumin, a pharmacologically safe phytochemical agent, on AGE induced tumor necrosis factor-a (TNF-a) and matrix metalloproteinase-13 (MMP-13) in rabbit chondrocytes ... Results : Curcumin significantly decreased AGE stimulated TNF-a and MMP-13 mRNA and suppressed the NF-?B activation via inhibition of ?Ba ( I-?Ba ) phosphorylation, I-?Ba degradation and p65 nuclear translocation
Kyo et al., Phytomedicine 1998 : Consequently, AGE stimulated the proliferation of mouse spleen cells and the release of cytokines, such as IL-2, TNF-alpha and IFN-gamma, increased NK activities, and enhanced phagocytosis of peritoneal macrophages
Vlassara et al., Prog Clin Biol Res 1989 (Diabetes Mellitus) : Coupling of AGE-proteins to their AGE-receptor results in TNF and IL-1 synthesis and secretion