PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11576850-10 2001 Sodium salicylate, a drug reported to inhibit the beta-subunit of IkappaB kinase (IKK), appeared to competitively inhibit TNF production by DMXAA in the presence of anti-CD14 antibody. Sodium Salicylate 0-17 tumor necrosis factor Homo sapiens 122-125 12067303-11 2002 TNF-induced IkappaBalpha degradation was inhibited by the proteasome inhibitor N-cbz-Leu-Leu-leucinal (MG-132) and a non-steroidal anti-inflammatory drug sodium salicylate (NaSal). Sodium Salicylate 154-171 tumor necrosis factor Homo sapiens 0-3 10199558-6 1999 To investigate the potential role of NFkappaB in this TNFalpha effect, we treated cells with sodium salicylate (NaS), an inhibitor of NFkappaB translocation. Sodium Salicylate 93-110 tumor necrosis factor Homo sapiens 54-62 10328874-4 1999 In addition, sodium salicylate and additional NSAIDs used at concentrations that activate HSF1 also inhibited the expression of other monocytic genes (TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, ICAM-1) activated by exposure to a pro-inflammatory stimulus (lipopolysaccharide, LPS). Sodium Salicylate 13-30 tumor necrosis factor Homo sapiens 151-160 9722548-9 1998 Induction of COX-2 and stimulation of COX activity by ET-1 and TNF-alpha were prevented by sodium salicylate and MG-132, suggesting that activation of NF-kappaB by either factor is needed for stimulation of COX-2. Sodium Salicylate 91-108 tumor necrosis factor Homo sapiens 63-72 9418855-0 1998 Activation of p38 mitogen-activated protein kinase by sodium salicylate leads to inhibition of tumor necrosis factor-induced IkappaB alpha phosphorylation and degradation. Sodium Salicylate 54-71 tumor necrosis factor Homo sapiens 95-116 8972019-0 1996 Acetylsalicylic acid and sodium salicylate inhibit LPS-induced NF-kappa B/c-Rel nuclear translocation, and synthesis of tissue factor (TF) and tumor necrosis factor alfa (TNF-alpha) in human monocytes. Sodium Salicylate 25-42 tumor necrosis factor Homo sapiens 171-180 8626494-0 1996 Inhibition of tumor necrosis factor-induced p42/p44 mitogen-activated protein kinase activation by sodium salicylate. Sodium Salicylate 99-116 tumor necrosis factor Homo sapiens 14-35 8626494-8 1996 In addition, the anti-inflammatory drug sodium salicylate, previously demonstrated to inhibit NF- kappaB activation by TNF, blocked the activation of p42/p44 MAPK in response to TNF but not in response to EGF. Sodium Salicylate 40-57 tumor necrosis factor Homo sapiens 119-122 8626494-8 1996 In addition, the anti-inflammatory drug sodium salicylate, previously demonstrated to inhibit NF- kappaB activation by TNF, blocked the activation of p42/p44 MAPK in response to TNF but not in response to EGF. Sodium Salicylate 40-57 tumor necrosis factor Homo sapiens 178-181 8626494-10 1996 Elucidation of the mechanism whereby sodium salicylate blocks TNF-induced p42/p44 MAPK activation may help to clarify TNF-activated signaling pathways. Sodium Salicylate 37-54 tumor necrosis factor Homo sapiens 62-65 8626494-10 1996 Elucidation of the mechanism whereby sodium salicylate blocks TNF-induced p42/p44 MAPK activation may help to clarify TNF-activated signaling pathways. Sodium Salicylate 37-54 tumor necrosis factor Homo sapiens 118-121 17646662-4 2007 Here, we reveal that sodium salicylate selectively enhances the apoptotic effects of TNF in human erythroleukemia cells but does not affect primary human lymphocytes or monocytes. Sodium Salicylate 21-38 tumor necrosis factor Homo sapiens 85-88 17646662-7 2007 Sodium salicylate achieved its effects by reducing the elevated NF-kappaB responsiveness and FLIP levels and restoring the apoptotic response of TNF rather than the proliferative/proinflammatory effects of the cytokine in these cancer cells. Sodium Salicylate 0-17 tumor necrosis factor Homo sapiens 145-148 17646662-9 2007 These findings expose that the enhanced proliferative nature of human leukemia cells is caused by elevated NF-kappaB and FLIP responses and basal levels, reversible by sodium salicylate to allow greater apoptotic responsiveness of cytotoxic stimuli such as TNF. Sodium Salicylate 168-185 tumor necrosis factor Homo sapiens 257-260 9096313-0 1997 Sodium salicylate induces apoptosis via p38 mitogen-activated protein kinase but inhibits tumor necrosis factor-induced c-Jun N-terminal kinase/stress-activated protein kinase activation. Sodium Salicylate 0-17 tumor necrosis factor Homo sapiens 90-111 9096313-1 1997 In a previous study, we demonstrated that sodium salicylate (NaSal) selectively inhibits tumor necrosis factor (TNF)-induced activation of the p42 and p44 mitogen-activated protein kinases (MAPKs) (known as extracellular signal-regulated kinases). Sodium Salicylate 42-59 tumor necrosis factor Homo sapiens 89-110 9096313-1 1997 In a previous study, we demonstrated that sodium salicylate (NaSal) selectively inhibits tumor necrosis factor (TNF)-induced activation of the p42 and p44 mitogen-activated protein kinases (MAPKs) (known as extracellular signal-regulated kinases). Sodium Salicylate 42-59 tumor necrosis factor Homo sapiens 112-115 27893782-8 2016 We determined co-treatment with metformin or sodium salicylate alone was successful in alleviating changes observed in feeding peptide mRNA regulation, whereas a preventative pre-treatment with metformin and sodium salicylate together was able to alleviate palmitate- and TNFalpha-induced induction of NPY and/or AgRP mRNA levels. Sodium Salicylate 208-225 tumor necrosis factor Homo sapiens 272-280 16432451-0 2006 Sodium salicylate inhibits TNF-alpha-induced NF-kappaB activation, cell migration, invasion and ICAM-1 expression in human melanoma cells. Sodium Salicylate 0-17 tumor necrosis factor Homo sapiens 27-36 16432451-2 2006 The aim of this study was to investigate the effect of the non-steroidal anti-inflammatory agent sodium salicylate on TNF-alpha-induced activation of the transcription factor nuclear factor-kappaB (NF-kappaB) and upregulation of intercellular adhesion molecule-1 (ICAM-1), and TNF-alpha-stimulated cell migration and invasion through fibronectin. Sodium Salicylate 97-114 tumor necrosis factor Homo sapiens 118-127 16432451-2 2006 The aim of this study was to investigate the effect of the non-steroidal anti-inflammatory agent sodium salicylate on TNF-alpha-induced activation of the transcription factor nuclear factor-kappaB (NF-kappaB) and upregulation of intercellular adhesion molecule-1 (ICAM-1), and TNF-alpha-stimulated cell migration and invasion through fibronectin. Sodium Salicylate 97-114 tumor necrosis factor Homo sapiens 277-286 16432451-5 2006 Sodium salicylate inhibited TNF-alpha-stimulated NF-kappaB activation in melanoma cells in a concentration-dependent manner, and this was achieved with pre-incubation times as short as 15 min. Sodium Salicylate 0-17 tumor necrosis factor Homo sapiens 28-37 16432451-6 2006 TNF-alpha-stimulated ICAM-1 expression in HBL cells was also downregulated by sodium salicylate, although in a manner inversely related to the concentration of this agent. Sodium Salicylate 78-95 tumor necrosis factor Homo sapiens 0-9 16432451-8 2006 In conclusion, sodium salicylate effectively inhibited TNF-alpha-induced upregulation of NF-kappaB, ICAM-1 expression, in-vitro migration and invasion in human melanoma cells, indicating that non-steroidal anti-inflammatory drugs may be a useful therapeutic approach to oppose inflammation-induced melanoma invasion and metastasis in vivo. Sodium Salicylate 15-32 tumor necrosis factor Homo sapiens 55-64