PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28638744-5	2017	Further, AZA significantly decreased human T-cell proliferation as well as IFNgamma and TNF-alpha serum levels, and reduced the expression of GRANZYME B and PERFORIN 1 by cytotoxic T cells.	Azacitidine	9-12	tumor necrosis factor	Homo sapiens	88-97	
21109971-3	2011	In several cancer cell lines, treatment with the DNA methyltransferase (Dnmt) inhibitor 5-Aza-dC effected expression of AID by TNF-alpha, and expression was further induced by additional treatment with histone deacetylase (HDAC) inhibitors with no stimulation.	Azacitidine	88-93	tumor necrosis factor	Homo sapiens	127-136	
26335173-5	2015	5-Aza-induced apoptosis was possibly due to induced expression of cytotoxic cytokines such as TNF-alpha.	Azacitidine	0-5	tumor necrosis factor	Homo sapiens	94-103	
26335173-6	2015	We revealed hypermethylation of the promoter region of TNF-alpha as a consequence of treatment with 5-aza.	Azacitidine	100-105	tumor necrosis factor	Homo sapiens	55-64	
26335173-8	2015	As a result, 5-aza inactivated Akt and inversely activated FOXO1, which contributed to the up-regulation of TNF-alpha.	Azacitidine	13-18	tumor necrosis factor	Homo sapiens	108-117	
26335173-9	2015	Furthermore, up-regulation of TNF-alpha by 5-aza administration was found in in vivo experiments.	Azacitidine	43-48	tumor necrosis factor	Homo sapiens	30-39	
21279994-10	2011	Levels of miR-203 did not change upon stimulation with IL-1beta, TNFalpha, or LPS; however, DNA demethylation with 5-azaC increased the expression of miR-203.	Azacitidine	115-121	tumor necrosis factor	Homo sapiens	65-73	
24297862-0	2014	Reducing TNF receptor 2+ regulatory T cells via the combined action of azacitidine and the HDAC inhibitor, panobinostat for clinical benefit in acute myeloid leukemia patients.	Azacitidine	71-82	tumor necrosis factor	Homo sapiens	9-12	
19877066-8	2009	The percentage CpG methylation was decreased by 5-aza-dC treatment but was reduced considerably more by IL-1beta and was almost abolished by TNFalpha/OSM.	Azacitidine	48-53	tumor necrosis factor	Homo sapiens	141-149	
18829727-4	2009	In a time- and concentration-dependent manner, primary murine, human hepatocytes and HepG2 cells exposed to 5-aza-CR became highly sensitive toward cell death induced by CD95L, tumor necrosis factor (TNF)-related apoptosis-inducing ligand, or TNF.	Azacitidine	108-116	tumor necrosis factor	Homo sapiens	200-203	
19117987-3	2009	Although 5-AZA-dC cannot fully induce differentiation, we show that 5-AZA-dC acts directly on TNFalpha-responsive promoters to facilitate TNFalpha-induced transcriptional pathways leading to differentiation.	Azacitidine	9-14	tumor necrosis factor	Homo sapiens	94-102	
19117987-3	2009	Although 5-AZA-dC cannot fully induce differentiation, we show that 5-AZA-dC acts directly on TNFalpha-responsive promoters to facilitate TNFalpha-induced transcriptional pathways leading to differentiation.	Azacitidine	9-14	tumor necrosis factor	Homo sapiens	138-146	
18829727-4	2009	In a time- and concentration-dependent manner, primary murine, human hepatocytes and HepG2 cells exposed to 5-aza-CR became highly sensitive toward cell death induced by CD95L, tumor necrosis factor (TNF)-related apoptosis-inducing ligand, or TNF.	Azacitidine	108-116	tumor necrosis factor	Homo sapiens	243-246	
1380648-0	1992	5-Azacytidine treatment of HA-A melanoma cells induces Sp1 activity and concomitant transforming growth factor alpha expression.	Azacitidine	0-13	tumor necrosis factor	Homo sapiens	84-116