PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24875677-4	2014	In order to evaluate if any polymorphism of potassium channels" genes could explain some of the "idiosyncratic" QT prolongations observed in patients treated with methadone, we tested the association between KCNE1, KCNE2, and KCNH2 polymorphism and the QT interval prolongation in those patients, controlling for other variables associated with a decrease of the repolarizing reserve.	Methadone	163-172	potassium voltage-gated channel subfamily H member 2	Homo sapiens	226-231	
24875677-9	2014	CONCLUSION: KCNH2 genotyping may be relevant in the analysis of cumulative risk factors for QT prolongation in patients on methadone maintenance treatment.	Methadone	123-132	potassium voltage-gated channel subfamily H member 2	Homo sapiens	12-17	
22381725-4	2012	Many explorations have helped in understanding the physiopathology by showing that opioids, including methadone, cause a blockage of the potassium channels of the gene HERG K+P.	Methadone	102-111	potassium voltage-gated channel subfamily H member 2	Homo sapiens	168-172	
18984955-9	2009	At 0.1, 0.3 and 1 mM, s-methadone reduced HERG current by 50 +/- 4, 76 +/- 5 and 87 +/- 5%, respectively, while r-methadone reduced HERG current by 26 +/- 4, 53 +/- 3 and 77 +/- 3%, respectively.	Methadone	22-33	potassium voltage-gated channel subfamily H member 2	Homo sapiens	42-46	
18984955-9	2009	At 0.1, 0.3 and 1 mM, s-methadone reduced HERG current by 50 +/- 4, 76 +/- 5 and 87 +/- 5%, respectively, while r-methadone reduced HERG current by 26 +/- 4, 53 +/- 3 and 77 +/- 3%, respectively.	Methadone	112-123	potassium voltage-gated channel subfamily H member 2	Homo sapiens	132-136	
15608471-6	2005	This data, associated with the finding that methadone is a rather potent inhibitor of HERG potassium channels and that it may induce torsade de pointes in predisposed subjects, supports the recommendation that patients entering methadone treatment (MT) are screened for cardiac risk factors.	Methadone	44-53	potassium voltage-gated channel subfamily H member 2	Homo sapiens	86-90	
12388652-2	2002	Our results show that LAAM, methadone, fentanyl, and buprenorphine were effective inhibitors of I(HERG), with IC(50) values in the 1 to 10 microM range.	Methadone	28-37	potassium voltage-gated channel subfamily H member 2	Homo sapiens	98-102	
14527710-6	2003	methadone causes QTc prolongation in humans; (2) whether methadone and/or chlorobutanol block cardiac HERG potassium currents (IHERG) in vitro.	Methadone	57-66	potassium voltage-gated channel subfamily H member 2	Homo sapiens	102-106	
12388652-6	2002	Further investigation showed that methadone block of I(HERG) was rapid, with steady-state inhibition achieved within 1 s when applied at its IC(50) concentration (10 microM) for I(HERG) block.	Methadone	34-43	potassium voltage-gated channel subfamily H member 2	Homo sapiens	55-59	
12388652-6	2002	Further investigation showed that methadone block of I(HERG) was rapid, with steady-state inhibition achieved within 1 s when applied at its IC(50) concentration (10 microM) for I(HERG) block.	Methadone	34-43	potassium voltage-gated channel subfamily H member 2	Homo sapiens	180-184	
12388652-9	2002	These results demonstrate that LAAM and methadone can block I(HERG) in transfected cells at clinically relevant concentrations, thereby providing a plausible mechanism for the adverse cardiac effects observed in some patients receiving LAAM or methadone.	Methadone	40-49	potassium voltage-gated channel subfamily H member 2	Homo sapiens	62-66	
12388652-9	2002	These results demonstrate that LAAM and methadone can block I(HERG) in transfected cells at clinically relevant concentrations, thereby providing a plausible mechanism for the adverse cardiac effects observed in some patients receiving LAAM or methadone.	Methadone	244-253	potassium voltage-gated channel subfamily H member 2	Homo sapiens	62-66