PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
33096612-0	2020	Chronic Valproic Acid Administration Increases Plasma, Liver, and Brain Ammonia Concentration and Suppresses Glutamine Synthetase Activity.	Valproic Acid	8-21	glutamate-ammonia ligase	Rattus norvegicus	109-129	
2865696-0	1985	Sodium valproate stimulates the particulate form of glutamine synthetase in rat brain.	Valproic Acid	0-16	glutamate-ammonia ligase	Rattus norvegicus	52-72	
7906715-0	1994	Valproate increases glutaminase and decreases glutamine synthetase activities in primary cultures of rat brain astrocytes.	Valproic Acid	0-9	glutamate-ammonia ligase	Rattus norvegicus	46-66	
7906715-5	1994	In astrocytes exposed to 1.2 mM valproate, glutaminase activity increased 80% by day 2 and remained elevated at day 4; glutamine synthetase activity was decreased 30%.	Valproic Acid	32-41	glutamate-ammonia ligase	Rattus norvegicus	119-139	
8450838-5	1993	Brain glutamate decarboxylase activity was significantly increased after incubation of the brain slices in the presence of valproate.	Valproic Acid	123-132	glutamate-ammonia ligase	Rattus norvegicus	6-29	
8450838-6	1993	Consequently, our results suggest that the mechanism of action of valproate is related to the increase in the levels of the inhibitory neurotransmitter GABA caused by the enhancement of flux through the glutamate decarboxylase-catalyzed reaction.	Valproic Acid	66-75	glutamate-ammonia ligase	Rattus norvegicus	203-226	
2865696-1	1985	The anticonvulsant drug, sodium valproate, enhanced total activity of glutamine synthetase in cortical and cerebellar homogenates of the rat at concentrations of 25-50 mM, without significantly altering substrate affinity.	Valproic Acid	25-41	glutamate-ammonia ligase	Rattus norvegicus	70-90