PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
1431902-4	1992	Thapsigargin treatment also decreased methacholine-induced secretion by about 30% in the presence of extracellular Ca2+ and essentially eliminated secretion that occurred independently of extracellular Ca2+ (which was about 30% of the secretory response that occurred in the presence of extracellular Ca2+).	Methacholine Chloride	38-50	carbonic anhydrase 2	Homo sapiens	115-118	
2663854-7	1989	In the absence of extracellular Ca2+, pretreatment with methacholine, an agonist believed to mobilize Ca2+ through the production of inositol 1,4,5-trisphosphate, inhibited but did not completely block the response to thapsigargin; likewise, pretreatment with thapsigargin inhibited the response to methacholine.	Methacholine Chloride	56-68	carbonic anhydrase 2	Homo sapiens	102-105	
2663854-11	1989	These results demonstrate that the mechanisms for activation of Ca2+ entry by thapsigargin and methacholine are the same and are consistent with the idea that entry is initiated by the depletion of the intracellular inositol 1,4,5-trisphosphate-sensitive Ca2+ pool.	Methacholine Chloride	95-107	carbonic anhydrase 2	Homo sapiens	64-67	
2663854-10	1989	In intact cells, methacholine and thapsigargin together produced a greater initial release of Ca2+ than either alone, but they were not additive in the sustained phase of Ca2+ mobilization.	Methacholine Chloride	17-29	carbonic anhydrase 2	Homo sapiens	94-97