PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17095614-3	2007	We used a surface expression assay to identify novel compounds that interfere with hERG trafficking and found that cardiac glycosides are potent inhibitors of hERG expression at the cell surface.	Glycosides	123-133	ETS transcription factor ERG	Homo sapiens	83-87	
6034759-3	1967	When the glycoside is placed on the receptor surface, in 7 min the ERG is completely eliminated by 10(-4)M ouabain and more than 90% inhibited by 3 x 10(-5)M ouabain.	Glycosides	9-18	ETS transcription factor ERG	Homo sapiens	67-70	
6034759-5	1967	The evidence suggests that abolition of the ERG by ouabain is due principally to inhibition of the active transport of sodium: (a) Structurally modified glycosides which are considerably less potent inhibitors of alkali cation-activated ATPase activity in preparations of frog retinal outer segments are also poorer inhibitors of electrical activity in isolated retinas.	Glycosides	153-163	ETS transcription factor ERG	Homo sapiens	44-47	
19139152-2	2009	One example of a clinically important compound class that potently inhibits hERG trafficking are cardiac glycosides.	Glycosides	105-115	ETS transcription factor ERG	Homo sapiens	76-80	
19139152-3	2009	We have shown previously that inhibition of hERG trafficking by cardiac glycosides is initiated via direct block of Na(+)/K(+) pumps and not via off-target interactions with hERG or any other protein.	Glycosides	72-82	ETS transcription factor ERG	Homo sapiens	44-48	
19139152-7	2009	Our data suggest a novel mechanism for drug-induced trafficking inhibition in which cardiac glycosides produce a [K(+)](i)-mediated conformational defect directly in the hERG channel protein.	Glycosides	92-102	ETS transcription factor ERG	Homo sapiens	170-174	
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.	Glycosides	14-24	ETS transcription factor ERG	Homo sapiens	98-102	
17095614-3	2007	We used a surface expression assay to identify novel compounds that interfere with hERG trafficking and found that cardiac glycosides are potent inhibitors of hERG expression at the cell surface.	Glycosides	123-133	ETS transcription factor ERG	Homo sapiens	159-163	
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.	Glycosides	89-99	ETS transcription factor ERG	Homo sapiens	166-170	
17095614-6	2007	hERG trafficking inhibition was initiated by cardiac glycosides through direct block of Na(+)/K(+) pumps and not via off-target interactions with hERG or another closely associated protein in its processing or export pathway.	Glycosides	53-63	ETS transcription factor ERG	Homo sapiens	0-4