PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28596183-3	2017	One key question is whether intestinal NAPEs act directly on cognate receptors or first require conversion to N-acylethanolamides (NAEs) by NAPE-hydrolyzing phospholipase D (NAPE-PLD).	n-acylethanolamides	110-129	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	140-172
28665150-6	2017	N-acylethanolamides (NAEs) are endogenous fatty acid substances that bind to PPAR-alpha and -gamma.	n-acylethanolamides	0-19	peroxisome proliferator activated receptor alpha	Homo sapiens	77-87
28596183-3	2017	One key question is whether intestinal NAPEs act directly on cognate receptors or first require conversion to N-acylethanolamides (NAEs) by NAPE-hydrolyzing phospholipase D (NAPE-PLD).	n-acylethanolamides	110-129	N-acyl phosphatidylethanolamine phospholipase D	Mus musculus	174-182
15289450-1	2004	Given the recent demonstration that oleoylethanolamide (OEA), a cannabinoid receptor-inactive N-acylethanolamine, decreases food intake by activating the nuclear receptor PPARalpha (peroxisome proliferator-activated receptor alpha) in the periphery, we here evaluated the effects of both saturated and unsaturated C18 N-acylethanolamides (C18:0; C18:1; C18:2) in mice feeding behavior after overnight starvation.	n-acylethanolamides	318-337	peroxisome proliferator activated receptor alpha	Mus musculus	171-180
15289450-1	2004	Given the recent demonstration that oleoylethanolamide (OEA), a cannabinoid receptor-inactive N-acylethanolamine, decreases food intake by activating the nuclear receptor PPARalpha (peroxisome proliferator-activated receptor alpha) in the periphery, we here evaluated the effects of both saturated and unsaturated C18 N-acylethanolamides (C18:0; C18:1; C18:2) in mice feeding behavior after overnight starvation.	n-acylethanolamides	318-337	peroxisome proliferator activated receptor alpha	Mus musculus	182-230
33021744-6	2020	We show that glycolysis is required to maintain the plasma membrane potential and that plasma membrane depolarization blocks cellular uptake of N-acylethanolamides-lipoprotein-borne Hh pathway inhibitors required for Smo destabilization.	n-acylethanolamides	144-163	hedgehog	Drosophila melanogaster	182-184
33021744-6	2020	We show that glycolysis is required to maintain the plasma membrane potential and that plasma membrane depolarization blocks cellular uptake of N-acylethanolamides-lipoprotein-borne Hh pathway inhibitors required for Smo destabilization.	n-acylethanolamides	144-163	smoothened	Drosophila melanogaster	217-220
34791641-1	2022	BACKGROUND AND PURPOSE: N-acylethanolamine acid amidase (NAAA) is a lysosomal enzyme accountable for the breakdown of N-acylethanolamides (NAEs) and its pharmacological inhibition determines beneficial effects in inflammatory conditions.	n-acylethanolamides	118-137	N-acylethanolamine acid amidase	Homo sapiens	24-55
34791641-1	2022	BACKGROUND AND PURPOSE: N-acylethanolamine acid amidase (NAAA) is a lysosomal enzyme accountable for the breakdown of N-acylethanolamides (NAEs) and its pharmacological inhibition determines beneficial effects in inflammatory conditions.	n-acylethanolamides	118-137	N-acylethanolamine acid amidase	Homo sapiens	57-61