PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24866131-6	2014	Additionally, the combined effects of serelaxin and enalapril reduced cardiac fibrosis by at least 2-fold compared with enalapril alone, when administered preventatively or therapeutically; by suppressing transforming growth factor-beta1 expression and phosphorylation of Smad2 (an intracellular regulator of transforming growth factor-beta1 activity; both P<0.05 versus enalapril alone) to a greater extent.	Enalapril	52-61	transforming growth factor beta 1	Homo sapiens	205-237	
24866131-6	2014	Additionally, the combined effects of serelaxin and enalapril reduced cardiac fibrosis by at least 2-fold compared with enalapril alone, when administered preventatively or therapeutically; by suppressing transforming growth factor-beta1 expression and phosphorylation of Smad2 (an intracellular regulator of transforming growth factor-beta1 activity; both P<0.05 versus enalapril alone) to a greater extent.	Enalapril	52-61	transforming growth factor beta 1	Homo sapiens	309-341	
25772062-3	2015	Since insulin-like growth factor (IGF-I) and transforming growth factor beta 1 (TGF-beta1) are the most potent stimulators of both collagen biosynthesis and prolidase activity, and prolidase is regulated by beta1 integrin signaling, the effect of enalapril and enalaprilat on IGF-IR, TGF-beta1, and beta1 integrin receptor expressions was evaluated.	Enalapril	247-256	transforming growth factor beta 1	Homo sapiens	45-78	
25772062-3	2015	Since insulin-like growth factor (IGF-I) and transforming growth factor beta 1 (TGF-beta1) are the most potent stimulators of both collagen biosynthesis and prolidase activity, and prolidase is regulated by beta1 integrin signaling, the effect of enalapril and enalaprilat on IGF-IR, TGF-beta1, and beta1 integrin receptor expressions was evaluated.	Enalapril	247-256	transforming growth factor beta 1	Homo sapiens	80-89	
25772062-8	2015	The exposure of the cells to 0.5 mM enalapril and enalaprilat contributed to increase in IGF-IR and alpha2beta1 integrin receptor as well as TGF-beta1 and NF-kappaB p65 expressions.	Enalapril	36-45	transforming growth factor beta 1	Homo sapiens	141-150	
25772062-9	2015	Enalapril- and enalaprilat-dependent increase of collagen biosynthesis in fibroblasts results from increase of prolidase activity and expression, which may undergo through activation of alpha2beta1 integrin and IGF-IR signaling as well as upregulation of TGF-beta1 and NF-kappaB p65, the inhibitor of collagen gene expression.	Enalapril	0-9	transforming growth factor beta 1	Homo sapiens	255-264	
10760085-3	2000	Using this target, we found that treatment with the angiotensin I-converting enzyme inhibitor enalapril or the Ang II type 1 receptor antagonist losartan reduced TGF-beta overexpression more effectively at doses clearly higher than those required to control blood pressure.	Enalapril	94-103	transforming growth factor beta 1	Homo sapiens	162-170	
10760085-11	2000	RESULTS: Compared with untreated nephritic animals on a normal-protein diet, a single treatment with enalapril, losartan, or low-protein diet significantly reduced glomerular TGF-beta production, albeit to a similar degree of approximately 45%.	Enalapril	101-110	transforming growth factor beta 1	Homo sapiens	175-183	
10760085-12	2000	A moderate, but significant further reduction in pathological TGF-beta expression of a total of 65% for enalapril and 60% for losartan was achieved when these drugs were combined with low-protein feeding.	Enalapril	104-113	transforming growth factor beta 1	Homo sapiens	62-70