PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20009079-0	2009	Alpha1-syntrophin mutations identified in sudden infant death syndrome cause an increase in late cardiac sodium current.	Sodium	105-111	syntrophin alpha 1	Homo sapiens	0-17	
27028743-0	2016	alpha1-Syntrophin Variant Identified in Drug-Induced Long QT Syndrome Increases Late Sodium Current.	Sodium	85-91	syntrophin alpha 1	Homo sapiens	0-17	
27028743-3	2016	We tested whether a novel SNTA1 (alpha1-syntrophin) variant (p.E409Q) found in a patient with diLQTS increases late sodium current (INa-L), thereby providing a disease mechanism.	Sodium	116-122	syntrophin alpha 1	Homo sapiens	26-31	
27028743-3	2016	We tested whether a novel SNTA1 (alpha1-syntrophin) variant (p.E409Q) found in a patient with diLQTS increases late sodium current (INa-L), thereby providing a disease mechanism.	Sodium	116-122	syntrophin alpha 1	Homo sapiens	33-50	
24319568-1	2011	The SNTA1-encoded alpha1-syntrophin (SNTA1) missense mutation, p.A257G, causes long QT syndrome (LQTS) by pathogenic accentuation of Nav1.5"s sodium current (INa).	Sodium	142-148	syntrophin alpha 1	Homo sapiens	4-9	
24319568-1	2011	The SNTA1-encoded alpha1-syntrophin (SNTA1) missense mutation, p.A257G, causes long QT syndrome (LQTS) by pathogenic accentuation of Nav1.5"s sodium current (INa).	Sodium	142-148	syntrophin alpha 1	Homo sapiens	18-35	
24319568-1	2011	The SNTA1-encoded alpha1-syntrophin (SNTA1) missense mutation, p.A257G, causes long QT syndrome (LQTS) by pathogenic accentuation of Nav1.5"s sodium current (INa).	Sodium	142-148	syntrophin alpha 1	Homo sapiens	37-42	
20009079-3	2009	We recently implicated mutations in alpha1-syntrophin (SNTA1) as a novel cause of long-QT syndrome, whereby mutant SNTA1 released inhibition of associated neuronal nitric oxide synthase by the plasma membrane Ca-ATPase PMCA4b, causing increased peak and late sodium current (I(Na)) via S-nitrosylation of the cardiac sodium channel.	Sodium	259-265	syntrophin alpha 1	Homo sapiens	36-53	
20009079-3	2009	We recently implicated mutations in alpha1-syntrophin (SNTA1) as a novel cause of long-QT syndrome, whereby mutant SNTA1 released inhibition of associated neuronal nitric oxide synthase by the plasma membrane Ca-ATPase PMCA4b, causing increased peak and late sodium current (I(Na)) via S-nitrosylation of the cardiac sodium channel.	Sodium	259-265	syntrophin alpha 1	Homo sapiens	55-60	
20009079-3	2009	We recently implicated mutations in alpha1-syntrophin (SNTA1) as a novel cause of long-QT syndrome, whereby mutant SNTA1 released inhibition of associated neuronal nitric oxide synthase by the plasma membrane Ca-ATPase PMCA4b, causing increased peak and late sodium current (I(Na)) via S-nitrosylation of the cardiac sodium channel.	Sodium	259-265	syntrophin alpha 1	Homo sapiens	115-120	
18591664-7	2008	A390V-SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase was partially inhibited by NOS blockers.	Sodium	97-103	syntrophin alpha 1	Homo sapiens	6-11	
18591664-8	2008	Expression of A390V-SNTA1 in cardiac myocytes also increased late sodium current.	Sodium	66-72	syntrophin alpha 1	Homo sapiens	20-25	
18591664-10	2008	These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene.	Sodium	92-98	syntrophin alpha 1	Homo sapiens	27-32	
18591664-10	2008	These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene.	Sodium	92-98	syntrophin alpha 1	Homo sapiens	124-129