PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30646605-1	2019	Metformin has been shown to inhibit glutaminase (GLS) activity and ammonia accumulation thereby reducing the risk of hepatic encephalopathy in type 2 diabetic patients.	Metformin	0-9	glutaminase	Homo sapiens	36-47	
30646605-1	2019	Metformin has been shown to inhibit glutaminase (GLS) activity and ammonia accumulation thereby reducing the risk of hepatic encephalopathy in type 2 diabetic patients.	Metformin	0-9	glutaminase	Homo sapiens	49-52	
30646605-2	2019	Since tumour cells are addicted to glutamine and often show an overexpression of glutaminase, we hypothesize that the antitumoral mechanism of metformin could be ascribed to inhibition of GLS and reduction of ammonia and ammonia-induced autophagy.	Metformin	143-152	glutaminase	Homo sapiens	81-92	
30646605-2	2019	Since tumour cells are addicted to glutamine and often show an overexpression of glutaminase, we hypothesize that the antitumoral mechanism of metformin could be ascribed to inhibition of GLS and reduction of ammonia and ammonia-induced autophagy.	Metformin	143-152	glutaminase	Homo sapiens	188-191	
30646605-5	2019	Interestingly, GLS-silenced cells reproduce the effect of metformin treatment showing reduced MAP1LC3B-II and GABARAP as well as ammonia accumulation.	Metformin	58-67	glutaminase	Homo sapiens	15-18	
30646605-7	2019	In conclusion, our work demonstrates that the anti-tumoral action of metformin is due to the inhibition of glutaminase and autophagy and could be used to improve the efficacy of chemotherapy.	Metformin	69-78	glutaminase	Homo sapiens	107-118