PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	NAADP	118-163	Fas ligand (TNF superfamily, member 6)	Mus musculus	68-72	
20200208-3	2010	The hypothesis being tested is that CD38 signaling pathway mediates FasL-induced intracellular Ca(2+) release through nicotinic acid adenine dinucleotide phosphate (NAADP) in mouse coronary arterial myocytes (CAMs) and thereby produces vasoconstriction in coronary arteries.	NAADP	165-170	Fas ligand (TNF superfamily, member 6)	Mus musculus	68-72	
20200208-4	2010	HPLC analysis demonstrated that FasL markedly increased NAADP production in CAMs from wild-type mice (CD38(+/+)) but not in cells from CD38 knockout (CD38(-/-)) mice.	NAADP	56-61	Fas ligand (TNF superfamily, member 6)	Mus musculus	32-36	
20200208-9	2010	These results strongly indicate that the early response of CAMs to FasL is to increase intracellular Ca(2+) levels and enhance the vascular reactivity through stimulation of NAADP production and lysosome-associated two-phase Ca(2+) release in coronary arteries.	NAADP	174-179	Fas ligand (TNF superfamily, member 6)	Mus musculus	67-71