PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
15632187-5	2005	We have previously reported that a single mutation of Met(121) (helix III) markedly reduced the receptor-mediated inositol phosphate production upon stimulation by CCK.	Inositol Phosphates	114-132	cholecystokinin	Homo sapiens	164-167	
15632187-6	2005	Computational simulations predicted that residue 121 affected orientation of the C-terminal end of CCK, thus suggesting that the molecular complex with a reduced inositol phosphate production observed with the mutated CCK1R resembles that resulting from binding of JMV 180 to the WT-CCK1R.	Inositol Phosphates	162-180	cholecystokinin	Homo sapiens	99-102	
10438490-6	1999	This mutation decreased the affinity and the potency of CCK to produce total inositol phosphates 302-fold and 456-fold without affecting the expression of the mutant receptor.	Inositol Phosphates	77-96	cholecystokinin	Homo sapiens	56-59	
11773861-8	2002	V125I-CCK2 receptor high affinity sites exhibited a 2-fold enhanced binding affinity for CCK which was correlated to a slightly increased potency in coupling to inositol phosphate production.	Inositol Phosphates	161-179	cholecystokinin	Homo sapiens	6-9	
7903820-4	1993	The phospholipase C activity, i.e. the accumulation of inositol phosphates, was increased by CCK (100 nmol l-1) at 3.3 mmol l-1 glucose.	Inositol Phosphates	55-74	cholecystokinin	Homo sapiens	93-96	
9006937-7	1997	Residues Trp-39 and Gln-40 of the receptor were crucial for binding of the C-terminal nonapeptide of CCK as W39F and Q40N mutants demonstrated parallel decreases in both affinity and potency to induce accumulation of inositol phosphates (12.9- and 20.9-fold).	Inositol Phosphates	217-236	cholecystokinin	Homo sapiens	101-104	
21156802-3	2011	We found that CCK and gastrin, which are full agonists on CCK2R-induced inositol phosphate production, rapidly and abundantly stimulate internalization.	Inositol Phosphates	72-90	cholecystokinin	Homo sapiens	14-17	
2833886-3	1988	CCK caused a rapid increase in intracellular free Ca2+ concentration ([Ca2+]i) monitored by Quin-2 and markedly stimulated inositol phosphate accumulation in chief cells.	Inositol Phosphates	123-141	cholecystokinin	Homo sapiens	0-3