PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12829521-8	2003	Correspondingly, aspirin enhanced NO synthase activity (citrulline formation) and intracellular cyclic GMP accumulation in endothelial cells.	Aspirin	17-24	5'-nucleotidase, cytosolic II	Homo sapiens	103-106	
191476-3	1977	Enhanced accumulation of cyclic GMP produced by arachidonic or collagen was prevented by prior exposure of platelets to aspirin or indomethacin.	Aspirin	120-127	5'-nucleotidase, cytosolic II	Homo sapiens	32-35	
4362746-2	1974	Collagen increased and aspirin decreased the cyclic [(3)H]GMP concentration in platelets.	Aspirin	23-30	5'-nucleotidase, cytosolic II	Homo sapiens	58-61	
12829521-10	2003	CONCLUSIONS: Our data suggest that endothelial NO synthase is a site of action of aspirin and that the NO/cyclic GMP system assumes a crucial function in mediating the cytoprotective action of aspirin.	Aspirin	193-200	5'-nucleotidase, cytosolic II	Homo sapiens	113-116	
10903927-3	2000	Similarly, NO-aspirin (10-100 microM) was found to induce tolerance to its own cyclic GMP stimulatory action and to that of GTN.	Aspirin	14-21	5'-nucleotidase, cytosolic II	Homo sapiens	86-89	
11887863-0	2001	Aspirin protected the nitric oxide/cyclic GMP generating system in human peritoneum.	Aspirin	0-7	5'-nucleotidase, cytosolic II	Homo sapiens	42-45	
10903927-6	2000	Prolonged treatment with NO-aspirin causes down-regulation of the cellular cyclic GMP response, suggesting that tolerance may occur during therapy with NO-aspirin.	Aspirin	28-35	5'-nucleotidase, cytosolic II	Homo sapiens	82-85	
10903927-6	2000	Prolonged treatment with NO-aspirin causes down-regulation of the cellular cyclic GMP response, suggesting that tolerance may occur during therapy with NO-aspirin.	Aspirin	155-162	5'-nucleotidase, cytosolic II	Homo sapiens	82-85	
9579743-2	1998	The effect of the NSAIDs indomethacin, indoprofen, diclofenac and acetylsalicylic acid on the increase in guanosine 3":5"-cyclic monophosphate (cyclic GMP) induced by nitric oxide-donor agents was tested in human whole platelets and in platelet crude homogenate.	Aspirin	66-86	5'-nucleotidase, cytosolic II	Homo sapiens	151-154	
9579743-10	1998	Indomethacin (10 microM), indoprofen (30 microM), diclofenac (100 microM) and acetylsalicylic acid (1000 microM) showed a comparable efficacy in inhibiting platelet thromboxane B2 (TXB2) production, suggesting that the inhibitory effect of indomethacin and indoprofen on the increase in cyclic GMP induced by both NO-donors was not mediated by inhibition of cyclooxygenase.	Aspirin	78-98	5'-nucleotidase, cytosolic II	Homo sapiens	294-297	
21043859-1	1993	Increases in [cyclic-3",5"-GMP] in aspirin-treated platelet-rich plasma and washed platelet preparations resulted from stimulation by all excitatory agonists tested, and by other agents which induced aggregate formation.	Aspirin	35-42	5'-nucleotidase, cytosolic II	Homo sapiens	27-30