PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28777484-0	2018	5-Azacytidine specifically inhibits the NIH-3T3 PCD process induced by TNF-alpha and cycloheximide via affecting BCL-XL.	Azacitidine	0-13	tumor necrosis factor	Mus musculus	71-80	
28486212-6	2017	In addition, treatment with 5-AZA suppressed APAP-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and nitric oxide (NO), 5-AZA also reversed the upregulation of myeloperoxidase (MPO) in the liver of APAP-exposed mice.	Azacitidine	28-33	tumor necrosis factor	Mus musculus	72-99	
28486212-6	2017	In addition, treatment with 5-AZA suppressed APAP-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and nitric oxide (NO), 5-AZA also reversed the upregulation of myeloperoxidase (MPO) in the liver of APAP-exposed mice.	Azacitidine	28-33	tumor necrosis factor	Mus musculus	101-110	
19887673-3	2010	In the current study, we analyzed the effect of 5-azaC in T-cell function and observed that 5-azaC inhibits T-cell proliferation and activation, blocking cell cycle in the G(0) to G(1) phase and decreasing the production of proinflammatory cytokines such as tumor necrosis factor-alpha and interferon-gamma.	Azacitidine	92-98	tumor necrosis factor	Mus musculus	258-285	
28486212-6	2017	In addition, treatment with 5-AZA suppressed APAP-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and nitric oxide (NO), 5-AZA also reversed the upregulation of myeloperoxidase (MPO) in the liver of APAP-exposed mice.	Azacitidine	157-162	tumor necrosis factor	Mus musculus	72-99	
28486212-6	2017	In addition, treatment with 5-AZA suppressed APAP-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and nitric oxide (NO), 5-AZA also reversed the upregulation of myeloperoxidase (MPO) in the liver of APAP-exposed mice.	Azacitidine	157-162	tumor necrosis factor	Mus musculus	101-110	
25251587-7	2014	Macrophages with 5-aza-dC treatment had downregulated expression of genes involved in inflammation (TNF-alpha, IL-6, IL-1beta, and inducible nitric oxidase) and chemotaxis (CD62/L-selectin, chemokine [C-C motif] ligand 2/MCP-1 [CCL2/MCP-1], CCL5, CCL9, and CCL2 receptor CCR2).	Azacitidine	17-22	tumor necrosis factor	Mus musculus	100-109	
27685787-3	2016	Results of ELISA revealed that DAC and Aza significantly inhibited the production of TNF-alpha and IL-1beta and prevented LPS-induced elevation of myeloperoxidase and malondialdehyde levels in serum.	Azacitidine	39-42	tumor necrosis factor	Mus musculus	85-94	
16814255-10	2006	Finally, the increased levels of TLR4 observed in ES cells after treatment with 5-aza-dC or TSA confer responsiveness to LPS, as induction of IL-6 and TNFalpha mRNA was detected in endotoxin stimulated ES cells.	Azacitidine	80-85	tumor necrosis factor	Mus musculus	151-159	
2473862-3	1989	Further, the selected 3LL variants are gene-regulatory variants rather than cellular mutants, as upregulation of the TNF-alpha receptor by interferon-gamma (IFN-gamma) or 5"-azacytidine treatment resulted in an increased vulnerability of the selected 3LL variants to the killing activity of macrophages and TNF-alpha.	Azacitidine	171-185	tumor necrosis factor	Mus musculus	117-126	
11229441-0	1999	Heat shock and 5-azacytidine inhibit nitric oxide synthesis and tumor necrosis factor-alpha secretion in activated macrophages.	Azacitidine	15-28	tumor necrosis factor	Mus musculus	64-91	
11229441-3	1999	Although heat shock significantly decreased TNF-alpha secretion only at the initiation stage of macrophage stimulation, 5-azacytidine treatment resulted in a more prolonged reduction in the secretion of TNF-alpha.	Azacitidine	120-133	tumor necrosis factor	Mus musculus	203-212	
2140484-4	1990	However, flat revertants retransformed by 5-azacytidine, without concomitant reactivation of E1a, were resistant to TNF-alpha.	Azacitidine	42-55	tumor necrosis factor	Mus musculus	116-125	
2473862-3	1989	Further, the selected 3LL variants are gene-regulatory variants rather than cellular mutants, as upregulation of the TNF-alpha receptor by interferon-gamma (IFN-gamma) or 5"-azacytidine treatment resulted in an increased vulnerability of the selected 3LL variants to the killing activity of macrophages and TNF-alpha.	Azacitidine	171-185	tumor necrosis factor	Mus musculus	307-316