PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2920915-4	1989	The pancreatic protein responses to pentagastrin, reaching about 37% of CCK maximum, was also significantly reduced but this effect was less pronounced than that observed in tests with CCK-8 or bombesin stimulation.	Pentagastrin	36-48	cholecystokinin	Canis lupus familiaris	72-75	
10987993-4	2000	While sulfated CCK-8 given alone had no effect on acid secretion, it caused marked inhibition of the plateau response to submaximal pentagastrin.	Pentagastrin	132-144	cholecystokinin	Canis lupus familiaris	15-18	
2767271-3	1989	administration of cholecystokinin caused reciprocal reactions in the stomach: pentagastrin suppressed the motility of fundal part and activated the contractions of antral part, whereas cholecystokinin activated the contractions of fundal part and suppressed the motility of antral part of the stomach.	Pentagastrin	78-90	cholecystokinin	Canis lupus familiaris	18-33	
680593-7	1978	The different effects of pentagastrin and CCK on spike activity in these studies may have been a consequence of pentagastrin-stimulated gastric acid secretion.	Pentagastrin	112-124	cholecystokinin	Canis lupus familiaris	42-45	
3668449-3	1987	Peptides containing the intact COOH-terminal tetrapeptide amide of CCK (CCK-4, CCK-5, pentagastrin, CCK-8 and gastrin-17) all induced dose-dependent (0.1, 3 and 100 nmol/l) increases in calcitonin release (P less than 0.05, n = 4) with biphasic secretion during 6-min infusion periods.	Pentagastrin	86-98	cholecystokinin	Canis lupus familiaris	67-70