PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10395082-5	1999	[14C] uridine incorporation was significantly higher in cells incubated with ET-1 (95 +/- 12%) but not AVP (9 +/- 11%).	Carbon-14	1-4	endothelin 1	Rattus norvegicus	77-81	
10362678-11	1999	Double-label pulse-chase experiments using [3H]- and [14C]leucine demonstrated that the secretory response to ET-1, in contrast to the response to muscle stretch, is based on peptide other than newly synthesized or relatively newly stored ANF.	Carbon-14	54-57	endothelin 1	Rattus norvegicus	110-114	
10050072-4	1999	PLD activity, measured as phosphatidylethanol (PEt) production in vessels labelled with [3H] or [14C]myristate, was increased in a concentration- and time-dependent manner following ET-1 stimulation, as were [3H]PA levels, peaking at 10 min (ET-1 100 nM) and remaining above control levels for up to 20 min.	Carbon-14	97-100	endothelin 1	Rattus norvegicus	182-186	
10050072-9	1999	The PC-PLC inhibitor D609, 2.5 microg/ml, completely abolished the ET-1-induced increase in [14C]DAG without affecting the increase in [14C]PA, PLD activity or the contractile response.	Carbon-14	93-96	endothelin 1	Rattus norvegicus	67-71	
10050072-10	1999	In [14C]choline-labelled vessels, [14C]phosphocholine levels were increased by ET-1 with a similar time course to DAG production.	Carbon-14	4-7	endothelin 1	Rattus norvegicus	79-83	
10050072-10	1999	In [14C]choline-labelled vessels, [14C]phosphocholine levels were increased by ET-1 with a similar time course to DAG production.	Carbon-14	35-38	endothelin 1	Rattus norvegicus	79-83	
10050072-12	1999	The tyrosine kinase inhibitor tyrphostin A23 (100 microM) abolished ET-1-induced [3H]PA, [3H]PEt and [14C]DAG increases, whilst the negative analogue A1 was without effect.	Carbon-14	102-105	endothelin 1	Rattus norvegicus	68-72	
8587331-4	1995	The formation (0.5 h) of 14C-labeled phosphatidylethanol ([14C]PEth) in the presence of exogenous ethanol (0.5%) in [14C]palmitate prelabeled cells, which reflects the PLD activity, was increased 1.9- and 5.6-fold by ET-1 and phorbolester (PMA, 10(-6) M), respectively.	Carbon-14	25-28	endothelin 1	Rattus norvegicus	217-221	
1331845-1	1992	Endothelin-1 (ET) produces contraction of cerebral resistance vessels in vitro and in situ, but also is neuroactive causing increases in tissue energy metabolism as measured by [14C]deoxyglucose autoradiography in the intact rat brain.	Carbon-14	178-181	endothelin 1	Rattus norvegicus	0-12	
7509966-2	1993	Using the quantitative autoradiographic [14C]deoxyglucose technique, we documented that the neuroanatomical metabolic correlates of the ET-1-induced convulsions in rats are high rates of glucose utilization by structures near the site of LCV injection and throughout a diverse circuit of anatomically related brain regions.	Carbon-14	41-44	endothelin 1	Rattus norvegicus	136-140	
1331845-1	1992	Endothelin-1 (ET) produces contraction of cerebral resistance vessels in vitro and in situ, but also is neuroactive causing increases in tissue energy metabolism as measured by [14C]deoxyglucose autoradiography in the intact rat brain.	Carbon-14	178-181	endothelin 1	Rattus norvegicus	14-16	
1847059-1	1991	The abilities of endothelin-1 to cause cellular injury and to enhance the levels of inositol-1,4,5-triphosphate and the breakdown of [14C]arachidonate-labeled phospholipids have been examined in the isolated rat heart model.	Carbon-14	134-137	endothelin 1	Rattus norvegicus	17-29	
1855455-1	1991	Intravenous infusion (14 nmol/min) and lateral cerebral ventricular injection (9 pmol) of endothelin-1 increased rates of glucose utilization (quantitative autoradiographic [14C]deoxyglucose method) by 75-219% in pars intermedia and distalis of the rat pituitary gland.	Carbon-14	174-177	endothelin 1	Rattus norvegicus	90-102