PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26305530-9	2015	Treatment with 5-AZA-dC significantly suppressed the expression of alpha-SMA, FN, TGF-beta R2 and phosphorylation of Smad2/3 and inhibited RPE cell migration.	Azacitidine	15-20	SMAD family member 2	Homo sapiens	117-124	
26212015-8	2016	Such hypermethylation-dependent silencing and 5-aza-dC-mediated reactivation of GDF1-SMAD2/3 activity was conserved in human gastric cancer cells (P < 0.05).	Azacitidine	46-51	SMAD family member 2	Homo sapiens	85-92	
15108358-7	2004	Aza-treated ACs displayed less Smad2 and 3 and increased Smad1, 5, and Smurf2 protein and showed a loss of TGF-beta signaling on the P3TP-luciferase reporter.	Azacitidine	0-3	SMAD family member 2	Homo sapiens	31-42	
15108358-8	2004	Suggesting that Aza-induction of Smurf2 may be responsible for the loss of Smad2 and 3 protein via this pathway, immunoprecipitation and metabolic labeling experiments confirmed that Aza accelerated the ubiquitination and degradation of these targets.	Azacitidine	16-19	SMAD family member 2	Homo sapiens	75-80	
15108358-8	2004	Suggesting that Aza-induction of Smurf2 may be responsible for the loss of Smad2 and 3 protein via this pathway, immunoprecipitation and metabolic labeling experiments confirmed that Aza accelerated the ubiquitination and degradation of these targets.	Azacitidine	183-186	SMAD family member 2	Homo sapiens	75-80	
15108358-9	2004	Overall, Aza-treated ACs represent a novel model for the study of mechanisms that regulate maturational potential of articular cartilage, with the data suggesting that maturation of these cells may be due to up-regulation of Smad1 and 5 coupled with a Smurf2-dependent degradation of Smad2 and 3 and loss of TGF-beta signaling.	Azacitidine	9-12	SMAD family member 2	Homo sapiens	284-295