PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
11514304-1	2001	Endothelial nitric oxide synthase (eNOS) is regulated both by caveolin-1 and 17beta-estradiol (E(2)).	Estradiol	77-93	nitric oxide synthase 3	Bos taurus	0-33	
10535965-7	1999	These findings stand in sharp contrast to the mechanism by which bradykinin, estradiol, and other mediators acutely activate eNOS, in which a rapid, agonist-promoted increase in intracellular calcium is required.	Estradiol	77-86	nitric oxide synthase 3	Bos taurus	125-129	
10077589-0	1999	Estradiol induces the calcium-dependent translocation of endothelial nitric oxide synthase.	Estradiol	0-9	nitric oxide synthase 3	Bos taurus	57-90	
10077589-2	1999	Using quantitative immunofluorescence imaging approaches, we have investigated the effect of estradiol on the subcellular targeting of endothelial nitric oxide synthase (eNOS) in bovine aortic endothelial cells.	Estradiol	93-102	nitric oxide synthase 3	Bos taurus	135-168	
10077589-2	1999	Using quantitative immunofluorescence imaging approaches, we have investigated the effect of estradiol on the subcellular targeting of endothelial nitric oxide synthase (eNOS) in bovine aortic endothelial cells.	Estradiol	93-102	nitric oxide synthase 3	Bos taurus	170-174	
10077589-4	1999	Within 5 min after the addition of estradiol, most of the eNOS translocates from the membrane to intracellular sites close to the nucleus.	Estradiol	35-44	nitric oxide synthase 3	Bos taurus	58-62	
10077589-8	1999	After estradiol addition, a transient rise in intracellular Ca2+ concentration precedes eNOS translocation.	Estradiol	6-15	nitric oxide synthase 3	Bos taurus	88-92	
10077589-9	1999	Both the Ca2+-mobilizing and eNOS-translocating effects of estradiol are completely blocked by the estrogen receptor antagonist ICI 182,780, and the intracellular Ca2+ chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid (BAPTA) prevents estradiol-induced eNOS translocation.	Estradiol	59-68	nitric oxide synthase 3	Bos taurus	29-33	
10077589-9	1999	Both the Ca2+-mobilizing and eNOS-translocating effects of estradiol are completely blocked by the estrogen receptor antagonist ICI 182,780, and the intracellular Ca2+ chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid (BAPTA) prevents estradiol-induced eNOS translocation.	Estradiol	59-68	nitric oxide synthase 3	Bos taurus	270-274	
10077589-9	1999	Both the Ca2+-mobilizing and eNOS-translocating effects of estradiol are completely blocked by the estrogen receptor antagonist ICI 182,780, and the intracellular Ca2+ chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid (BAPTA) prevents estradiol-induced eNOS translocation.	Estradiol	252-261	nitric oxide synthase 3	Bos taurus	29-33	
10077589-10	1999	Use of the nitric oxide-specific dye diaminofluorescein shows that estradiol treatment increases nitric oxide generation by endothelial cells; this response is blocked by ICI 182,780 and by the eNOS inhibitor Nomega-nitro-L-arginine.	Estradiol	67-76	nitric oxide synthase 3	Bos taurus	194-198	
10077589-11	1999	These results show that estradiol induces subcellular translocation of eNOS by a rapid, Ca2+-dependent, receptor-mediated mechanism, and they suggest a nongenomic role for estrogen in the modulation of NO-dependent vascular tone.	Estradiol	24-33	nitric oxide synthase 3	Bos taurus	71-75