PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21995308-3	2011	As detected both on mRNA and protein levels, dimethylfumarate effected a profound reduction of TNFalpha-induced expression of E-selectin (CD62E), ICAM-1 (CD54) and VCAM-1 (CD106) on two different endothelial cell populations in a concentration-dependent manner.	Dimethyl Fumarate	45-61	selectin E	Homo sapiens	126-136	
21995308-3	2011	As detected both on mRNA and protein levels, dimethylfumarate effected a profound reduction of TNFalpha-induced expression of E-selectin (CD62E), ICAM-1 (CD54) and VCAM-1 (CD106) on two different endothelial cell populations in a concentration-dependent manner.	Dimethyl Fumarate	45-61	selectin E	Homo sapiens	138-143	
11886496-0	2001	Dimethylfumarate inhibits tumor-necrosis-factor-induced CD62E expression in an NF-kappa B-dependent manner.	Dimethyl Fumarate	0-16	selectin E	Homo sapiens	56-61	
17671516-8	2008	DMF led to a significant reduction in binding of human peripheral blood mononuclear cells (PBMCs) to E-selectin (72%), P-selectin (36%), and vascular cell adhesion molecule-1 (33%) in vitro.	Dimethyl Fumarate	0-3	selectin E	Homo sapiens	101-111	
11886496-4	2001	Using human umbilical vein endothelial cells, dimethylfumarate almost completely inhibited tumor-necrosis-factor-induced CD62E, but not CD54 expression at concentrations < or = 70 microM, mimicking the situation in vivo.	Dimethyl Fumarate	46-62	selectin E	Homo sapiens	121-126	
11886496-5	2001	A 60 min dimethylfumarate preincubation was sufficient to block tumor-necrosis-factor-induced CD62E expression for up to 24 h. In contrast, equimolar concentrations of methylhydrogenfumarate, the hydrolysis product of dimethylfumarate, did not suppress tumor-necrosis-factor-induced CD62E expression.	Dimethyl Fumarate	9-25	selectin E	Homo sapiens	94-99	
11886496-5	2001	A 60 min dimethylfumarate preincubation was sufficient to block tumor-necrosis-factor-induced CD62E expression for up to 24 h. In contrast, equimolar concentrations of methylhydrogenfumarate, the hydrolysis product of dimethylfumarate, did not suppress tumor-necrosis-factor-induced CD62E expression.	Dimethyl Fumarate	9-25	selectin E	Homo sapiens	283-288	
11886496-7	2001	Using CD62E, NF-kappa B, or AP-1-responsive promoter constructs, dimethylfumarate inhibited tumor-necrosis-factor-induced activation of the CD62E and the NF-kappa B but not the AP-1 promoter construct.	Dimethyl Fumarate	65-81	selectin E	Homo sapiens	6-11	
11886496-7	2001	Using CD62E, NF-kappa B, or AP-1-responsive promoter constructs, dimethylfumarate inhibited tumor-necrosis-factor-induced activation of the CD62E and the NF-kappa B but not the AP-1 promoter construct.	Dimethyl Fumarate	65-81	selectin E	Homo sapiens	140-145	
11886496-8	2001	In summary, at a dose range < or = 70 microM, dimethylfumarate appeared to be a specific inhibitor of CD62E expression in an NF-kappa B-dependent manner.	Dimethyl Fumarate	49-65	selectin E	Homo sapiens	105-110	
9168952-0	1997	Dimethylfumarate is an inhibitor of cytokine-induced E-selectin, VCAM-1, and ICAM-1 expression in human endothelial cells.	Dimethyl Fumarate	0-16	selectin E	Homo sapiens	53-63	
9168952-3	1997	Dimethylfumarate inhibited ICAM-1, VCAM-1, and E-selectin expression and reduced adhesion of U937 cells to stimulated HUVEC.	Dimethyl Fumarate	0-16	selectin E	Homo sapiens	47-57