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