PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29592879-0	2018	Itraconazole-Induced Inhibition on Human Esophageal Cancer Cell Growth Requires AMPK Activation.	Itraconazole	0-12	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	80-84	
29592879-3	2018	Itraconazole activated AMPK signaling, which was required for subsequent esophageal cancer cell death.	Itraconazole	0-12	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	23-27	
29592879-4	2018	Pharmacologic AMPK inhibition, AMPKalpha1 shRNA, or dominant negative mutation (T172A) almost completely abolished itraconazole-induced cytotoxicity against esophageal cancer cells.	Itraconazole	115-127	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	14-18	
29592879-5	2018	Significantly, itraconazole induced AMPK-dependent autophagic cell death (but not apoptosis) in esophageal cancer cells.	Itraconazole	15-27	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	36-40	
29592879-6	2018	Furthermore, AMPK activation by itraconazole induced multiple receptor tyrosine kinases (RTKs: EGFR, PDGFRalpha, and PDGFRbeta), lysosomal translocation, and degradation to inhibit downstream Akt activation.	Itraconazole	32-44	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	13-17	
29592879-10	2018	AMPK activation, RTK degradation, and Akt inhibition were observed in itraconazole-treated tumors.	Itraconazole	70-82	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	0-4	
29592879-11	2018	Together, itraconazole inhibits esophageal cancer cell growth via activating AMPK signaling.	Itraconazole	10-22	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	77-81