PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8843772-5	1996	In contrast, a MAb specific for the common COOH-terminal pentapeptide of gastrin and CCK inhibited gastrin-17- and pentagastrin-stimulated gastric acid secretion and CCK-stimulated pancreatic secretion.	Pentagastrin	115-127	gastrin	Rattus norvegicus	73-80	
8791971-7	1996	Similarly, the putative CCKB-gastrin-antagonist, spiroglumide, proved to be capable of inhibiting dose-dependently pentagastrin-induced acid hypersecretion, its ID50 being 20.1 (8.67-46.4) mg/kg.	Pentagastrin	115-127	gastrin	Rattus norvegicus	29-36	
8225230-2	1993	Both gastrin fragments inhibited triacylglycerol release in a biphasic manner, exhibiting maximal effect at 0.1 nmol/L (nonsulfated heptadecagastrin) and 0.3 nmol/L (pentagastrin).	Pentagastrin	166-178	gastrin	Rattus norvegicus	5-12	
7491961-10	1995	These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats.	Pentagastrin	147-159	gastrin	Rattus norvegicus	37-44	
7883218-2	1995	The hypothesis that gastrin is trophic throughout the gut was tested by giving three doses of pentagastrin and one of gastrin 17 to rats maintained by total parenteral nutrition (TPN).	Pentagastrin	94-106	gastrin	Rattus norvegicus	20-27	
8483804-4	1993	We conclude: 1) pentagastrin stimulates acid secretion through a gastrin-type receptor, but CCK may not, and 2) pentagastrin and CCK can stimulate acid secretion despite simultaneous blockade of CCKB/gastrin and CCKA receptors.	Pentagastrin	16-28	gastrin	Rattus norvegicus	65-72	
1393262-4	1992	In RGM, gastrin peptides (sulphated gastrin heptadecapeptide (G-17), non-sulphated (ns) G-17 and pentagastrin) were potent agonists of acid secretion (EC50 values of 4.3, 16 and 27 nM respectively).	Pentagastrin	97-109	gastrin	Rattus norvegicus	8-15	
4053918-2	1985	Although pentagastrin has a tropic action on intestinal mucosa in suckling rat pups, and at weaning a rise in gastrin levels coincides with maturation of the intestinal mucosa, direct correlations of serum gastrin levels and intestinal maturation have yet to be made.	Pentagastrin	9-21	gastrin	Rattus norvegicus	110-117	
1714408-4	1991	Benzodiazepine receptor antagonists for gastrin (L-365,260) and for CCK (L-364,718) showed higher efficacy in the inhibition of amylase release induced by pentagastrin and CCK, respectively, but failed to affect that induced by bombesin.	Pentagastrin	155-167	gastrin	Rattus norvegicus	40-47	
1687371-4	1991	The novel CCKB/gastrin antagonists CI-988 and PD 136450, and L-365,260 dose-dependently inhibited pentagastrin-induced secretion.	Pentagastrin	98-110	gastrin	Rattus norvegicus	15-22	
6697369-11	1984	These observations are compatible with the hypothesis that (i) the primary effects of gastrin and pentagastrin on the proximal intestine are as secretogogues and effects on cell proliferation may be secondary, (ii) gastrin and pentagastrin at physiological levels do not stimulate small intestinal cell proliferation, however glucagon does, and (iii) gastrin at physiological levels and pentagastrin at pharmacological levels may stimulate cell proliferation in the colon.	Pentagastrin	227-239	gastrin	Rattus norvegicus	86-93	
6697369-11	1984	These observations are compatible with the hypothesis that (i) the primary effects of gastrin and pentagastrin on the proximal intestine are as secretogogues and effects on cell proliferation may be secondary, (ii) gastrin and pentagastrin at physiological levels do not stimulate small intestinal cell proliferation, however glucagon does, and (iii) gastrin at physiological levels and pentagastrin at pharmacological levels may stimulate cell proliferation in the colon.	Pentagastrin	227-239	gastrin	Rattus norvegicus	103-110	
6697369-11	1984	These observations are compatible with the hypothesis that (i) the primary effects of gastrin and pentagastrin on the proximal intestine are as secretogogues and effects on cell proliferation may be secondary, (ii) gastrin and pentagastrin at physiological levels do not stimulate small intestinal cell proliferation, however glucagon does, and (iii) gastrin at physiological levels and pentagastrin at pharmacological levels may stimulate cell proliferation in the colon.	Pentagastrin	227-239	gastrin	Rattus norvegicus	103-110	
6697369-11	1984	These observations are compatible with the hypothesis that (i) the primary effects of gastrin and pentagastrin on the proximal intestine are as secretogogues and effects on cell proliferation may be secondary, (ii) gastrin and pentagastrin at physiological levels do not stimulate small intestinal cell proliferation, however glucagon does, and (iii) gastrin at physiological levels and pentagastrin at pharmacological levels may stimulate cell proliferation in the colon.	Pentagastrin	227-239	gastrin	Rattus norvegicus	86-93	
6697369-11	1984	These observations are compatible with the hypothesis that (i) the primary effects of gastrin and pentagastrin on the proximal intestine are as secretogogues and effects on cell proliferation may be secondary, (ii) gastrin and pentagastrin at physiological levels do not stimulate small intestinal cell proliferation, however glucagon does, and (iii) gastrin at physiological levels and pentagastrin at pharmacological levels may stimulate cell proliferation in the colon.	Pentagastrin	227-239	gastrin	Rattus norvegicus	103-110	
6697369-11	1984	These observations are compatible with the hypothesis that (i) the primary effects of gastrin and pentagastrin on the proximal intestine are as secretogogues and effects on cell proliferation may be secondary, (ii) gastrin and pentagastrin at physiological levels do not stimulate small intestinal cell proliferation, however glucagon does, and (iii) gastrin at physiological levels and pentagastrin at pharmacological levels may stimulate cell proliferation in the colon.	Pentagastrin	227-239	gastrin	Rattus norvegicus	103-110	
6873393-1	1983	Chronic experiments in dogs with isolated loop of the small intestine and acute experiments in rats revealed specific interrelationships between the gastrin and the cholinergic activity: pentagastrin potentiated its effects by activation of cholinergic processes in the intestinal mucosa (increasing the acetylcholin content and the cholinesterase activity).	Pentagastrin	187-199	gastrin	Rattus norvegicus	149-156	
224710-5	1979	In order to decrease the specific binding of gastrin by 50% the competitors in order of potency are 15-Leu G-17 greater than cholecystokinin greater than caerulein greater than pentagastrin; secretin did not display a response similar to the other four competitors tested, indicating that its inhibition may be non-competitive.	Pentagastrin	177-189	gastrin	Rattus norvegicus	45-52	
6408699-5	1983	The proliferation stimulating action of gastrin is also detectable at chronic oral application of N-Methyl-N"-nitroso-N-nitroguanidine for induction of stomach and intestinal tumors simultaneously to pentagastrin administration or partial stomach resection in the intact, tumor free oxyntic mucosa of stomach.	Pentagastrin	200-212	gastrin	Rattus norvegicus	40-47	
173424-5	1975	The results obtained suggest that the activation of carbonic anhydrase in vivo by gastrin (pentagastrin), histamine and 3",5"-AMP is due to the phosphorylation of highly active isoenzyme by 3",5-AMP-dependent protein kinase.	Pentagastrin	91-103	gastrin	Rattus norvegicus	82-89	
1023739-4	1976	It has been observed that labelled gastrin or pentagastrin activity reaches its peak in the plasma in the 5th minute after intravenous injection.	Pentagastrin	46-58	gastrin	Rattus norvegicus	35-42