PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17095614-4	2007	Further investigation of digitoxin, ouabain, and digoxin revealed that all three cardiac glycosides reduced expression of the fully glycosylated cell surface form of hERG on Western blots, indicating that channel exit from the endoplasmic reticulum is blocked.	Digitoxin	25-34	ETS transcription factor ERG	Homo sapiens	166-170	
17095614-9	2007	Thus, cardiac glycosides are able to delay cardiac repolarization at nanomolar concentrations via hERG trafficking inhibition, and this may contribute to the complex electrocardiographic changes seen with compounds such as digitoxin.	Digitoxin	223-232	ETS transcription factor ERG	Homo sapiens	98-102	
17095614-7	2007	In isolated guinea pig myocytes, long-term exposure to 30 nM of the clinically used drugs digoxin or digitoxin reduced hERG/rapidly activating delayed rectifier K(+) current (I(Kr)) currents by approximately 50%, whereas three other cardiac membrane currents--inward rectifier current, slowly activating delayed rectifier K(+) current, and calcium current--were not affected.	Digitoxin	101-110	ETS transcription factor ERG	Homo sapiens	119-123	
17095614-8	2007	Importantly, 100 nM digitoxin prolonged action potential duration on long-term exposure consistent with a reduction in hERG/I(Kr) channel number.	Digitoxin	20-29	ETS transcription factor ERG	Homo sapiens	119-123