PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14981072-10	2004	In Ca2+-free (2 mmol/L EGTA) Hank"s solution, ET-1 caused 15% cell contraction, with no increase in [Ca2+]i, and translocation of epsilon-PKC that were inhibited by epsilon-PKC V1-2 inhibitory peptide.	Egtazic Acid	23-27	endothelin 1	Homo sapiens	46-50	
19171135-6	2009	Endothelin-1-induced IL-6 production was markedly attenuated by EGTA and various Ca(2+) channel inhibitors such as 3,5-bis(trifluoromethyl)-1H-pyrazole derivative (BTP-2), 1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole hydrochloride (SKF96365), and nifedipine.	Egtazic Acid	64-68	endothelin 1	Homo sapiens	0-12	
15702350-9	2005	Intracellular EGTA abolished the transient increase by ET-1 and partially inhibited the subsequent decrease in the currents.	Egtazic Acid	14-18	endothelin 1	Homo sapiens	55-59	
9863648-5	1998	However, in the presence of 5 mM EGTA or SKF 96365, an inhibitor of receptor mediated Ca2+ influx (1.0-3.0 x 10(-5) M) ET-1-induced Ca2+ increases were inhibited in normal, but not in PTX-treated cells.	Egtazic Acid	33-37	endothelin 1	Homo sapiens	119-123	
14966371-0	2004	Thapsigargin and EGTA inhibit endothelin-1-induced glucose transport.	Egtazic Acid	17-21	endothelin 1	Homo sapiens	30-42	
14966371-3	2004	Among a variety of Ca(2+)-related agents tested, EGTA and thapsigargin were found to suppress both the glucose uptake and intracellular Ca(2+) mobilization induced by ET-1, as determined by Fura-2 analysis.	Egtazic Acid	49-53	endothelin 1	Homo sapiens	167-171	
11078432-4	2000	The sustained increase of cytosolic and nuclear Ca2+ by ET-1 in both EEC preparations was completely blocked by the calcium chelator ethylene glycol-bis (beta-aminoethylether)-N,N,N",N"-tetra-acetic acid (EGTA) but was insensitive to the L-type Ca2+ channel blocker, nifedipine.	Egtazic Acid	205-209	endothelin 1	Homo sapiens	56-60	
10919988-4	2000	With low ethyleneglycol-bis-(beta-aminoethyl ether)-N,N"-tetraacetic acid (EGTA) and K(+) internal solutions, both ET-1 and histamine induced a sustained depolarization from approximately -40 to -20 mV.	Egtazic Acid	9-73	endothelin 1	Homo sapiens	115-119	
10919988-4	2000	With low ethyleneglycol-bis-(beta-aminoethyl ether)-N,N"-tetraacetic acid (EGTA) and K(+) internal solutions, both ET-1 and histamine induced a sustained depolarization from approximately -40 to -20 mV.	Egtazic Acid	75-79	endothelin 1	Homo sapiens	115-119	
9426289-7	1998	Prior depletion of intracellular Ca2+ stores with thapsigargin, an inhibitor of Ca2+-ATPase of the endoplasmic reticulum, abolished the ET-1-induced Ca2+ transient, whereas removal of extracellular Ca2+ with EGTA eliminated the sustained rise.	Egtazic Acid	208-212	endothelin 1	Homo sapiens	136-140	
7923609-8	1994	Moreover, shear stress-induced ET-1 gene expression was inhibited by EGTA, BAPTA/AM, and staurosporine to a degree similar to the inhibition of actin depolymerization.	Egtazic Acid	69-73	endothelin 1	Homo sapiens	31-35	
9067893-8	1997	In contrast, ET-1-induced activation of JNK was significantly reduced by calcium chelation (with BAPTA/AM and EGTA).	Egtazic Acid	110-114	endothelin 1	Homo sapiens	13-17	
7598740-9	1995	The PKC activator phorbol 12-myristate 13-acetate (0.4 microM) stimulated ET-1 release 1.4-fold (P < 0.01) and its effect was abolished by EGTA (5 mM).	Egtazic Acid	142-146	endothelin 1	Homo sapiens	74-78	
8588187-4	1995	The ET-1 induced increase in [Ca2+]i was suppressed by 1 mM EGTA, a calcium chelating agent in the medium.	Egtazic Acid	60-64	endothelin 1	Homo sapiens	4-8	
7535782-10	1995	EGTA strongly inhibited the Et-1 gene expression.	Egtazic Acid	0-4	endothelin 1	Homo sapiens	28-32	
7921598-20	1994	Contraction induced by ET-1 was virtually abolished in Ca2+-free medium containing 0.1 mM EGTA, indicating that this response was dependent upon the influx of extracellular Ca2 .Contraction was inhibited by about 50% in the presence of nicardipine (1 MicroM), indicating that a significant component of this response was mediated via the activation of L-type Ca2+ channels.6.	Egtazic Acid	90-94	endothelin 1	Homo sapiens	23-27	
1658154-8	1991	In HDMEC incubated with 100 nM ET-1, inhibition of PGE2 release was unaffected by the dihydropyridine Ca++ channel antagonist nifedipine or the extracellular Ca++ chelator EGTA, whereas the intracellular Ca++ chelator TMB-8 partially blocked the action of ET-1.	Egtazic Acid	172-176	endothelin 1	Homo sapiens	31-35	
1725414-6	1991	cAMP accumulation, induced by 100 nM ET-1, was blocked by extracellular Ca2+ chelator EGTA, the intracellular Ca2+ chelator TMB-8, and dihydropyridine Ca(2+)-channel antagonist nifedipine (p less than 0.05), whereas ET-1 inhibition of PGE2 release was unaffected.	Egtazic Acid	86-90	endothelin 1	Homo sapiens	37-41	
2545192-2	1989	However, even in a Ca2+-free, EGTA-containing solution relatively high concentrations of ET1 induced a weak vasoconstriction, which was markedly but not completely inhibited by pretreatment with caffeine.	Egtazic Acid	30-34	endothelin 1	Homo sapiens	89-92