PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16113405-6	2004	In many epithelial tissues, amiloride-sensitive epithelial sodium channels (ENaC) are formed from three subunit proteins designated alpha-ENaC, beta-ENaC, and gamma-ENaC.	Amiloride	28-37	sodium channel epithelial 1 subunit gamma	Homo sapiens	159-169	
14576089-9	2004	These results are consistent with the hypothesis that a heterooligomer composed of alpha-, beta-, and gamma-ENaC may be the molecular basis of the native channels, which are responsible for amiloride-sensitive electrogenic Na+ absorption in rat rectal colon.	Amiloride	190-199	sodium channel epithelial 1 subunit gamma	Homo sapiens	102-112	
12030906-12	2002	CONCLUSIONS: The observed differences in RBC Na+,K+-ATPase activity and nasal PD response to amiloride between the two pairs of twins support the contention of different basic pathogenic mechanisms in the two forms of PHA1.	Amiloride	93-102	sodium channel epithelial 1 subunit gamma	Homo sapiens	218-222	
12381774-6	2002	In many epithelial tissues, amiloride-sensitive epithelial sodium channels (ENaC) are formed from three subunit proteins, designated alpha-, beta-, and gamma-ENaC.	Amiloride	28-37	sodium channel epithelial 1 subunit gamma	Homo sapiens	152-162	
9118951-1	1997	Pseudohypoaldosteronism type 1 (PHA-1) is an inherited disease characterized by severe neonatal salt-wasting and caused by mutations in subunits of the amiloride-sensitive epithelial sodium channel (ENaC).	Amiloride	152-161	sodium channel epithelial 1 subunit gamma	Homo sapiens	0-37	
9392872-7	1997	We have substantiated this possibility by using Northern analysis to identify in human ciliary body RNA a 3.7-kb transcript corresponding to the alpha-subunit of the amiloride-sensitive, alpha beta gamma-ENaC epithelial sodium channel.	Amiloride	166-175	sodium channel epithelial 1 subunit gamma	Homo sapiens	198-208	
11463765-1	2001	The SCNN1G gene, located on human chromosome 16p12, encodes the gamma subunit of the amiloride-sensitive epithelial sodium channel, and mutations in SCNN1G can result in Liddle"s syndrome or pseudohypoaldosteronism type I.	Amiloride	85-94	sodium channel epithelial 1 subunit gamma	Homo sapiens	4-10	
11344206-2	2001	There are 2 forms of PHA1: the autosomal recessive form with symptoms persisting into adulthood, caused by mutations in the amiloride-sensitive luminal sodium channel, and the autosomal dominant or sporadic form, which shows milder symptoms that remit with age.	Amiloride	124-133	sodium channel epithelial 1 subunit gamma	Homo sapiens	21-25	
31018202-2	2019	Mutations in the genes encoding the amiloride-sensitive epithelial sodium channel, ENaC, account for genetic causes of systemic PHA1.	Amiloride	36-45	sodium channel epithelial 1 subunit gamma	Homo sapiens	128-132	
8640238-4	1996	These two chromosomal regions harbour the genes encoding the three subunits of the human amiloride sensitive epithelial sodium channel (hENaC): SCNN1B and SCNN1G on 16p and SCNN1A on 12p.	Amiloride	89-98	sodium channel epithelial 1 subunit gamma	Homo sapiens	155-161	
18990692-3	2009	In Xenopus oocytes expressing human alpha-, beta-, and gammaENaC, amiloride-sensitive current was altered by protons in the physiologically relevant range (pH 8.5-6.0).	Amiloride	66-75	sodium channel epithelial 1 subunit gamma	Homo sapiens	36-64	
26807262-11	2016	LEARNING POINTS: PHA1 is a rare genetic condition, causing functional abnormalities of the amiloride-sensitive ENaC.PHA1 was caused by previously unreported SCNN1B gene mutations (c.1288delC and c.1466+1 G>A).Early recognition of this condition and adherence to symptomatic therapy is important, as the electrolyte abnormalities found may lead to severe dehydration, cardiac arrhythmias and even death.High doses of sodium polystyrene sulfonate, sodium chloride and sodium bicarbonate are required for symptomatic treatment.	Amiloride	91-100	sodium channel epithelial 1 subunit gamma	Homo sapiens	17-21	
26807262-11	2016	LEARNING POINTS: PHA1 is a rare genetic condition, causing functional abnormalities of the amiloride-sensitive ENaC.PHA1 was caused by previously unreported SCNN1B gene mutations (c.1288delC and c.1466+1 G>A).Early recognition of this condition and adherence to symptomatic therapy is important, as the electrolyte abnormalities found may lead to severe dehydration, cardiac arrhythmias and even death.High doses of sodium polystyrene sulfonate, sodium chloride and sodium bicarbonate are required for symptomatic treatment.	Amiloride	91-100	sodium channel epithelial 1 subunit gamma	Homo sapiens	116-120	
19344080-4	2009	PHA1 is caused by mutations in genes encoding either subunits of the amiloride-sensitive epithelial sodium channel (ENaC) or mineralocorticoid receptor (MR) inherited in an autosomal recessive or dominant form, respectively.	Amiloride	69-78	sodium channel epithelial 1 subunit gamma	Homo sapiens	0-4	
16630545-1	2006	Liddle"s syndrome (excessive absorption of sodium ions) and PHA-1 (pseudohypoaldosteronism type 1) with decreased sodium absorption are caused by the mutations in the amiloride-sensitive epithelial sodium channel ENaC.	Amiloride	167-176	sodium channel epithelial 1 subunit gamma	Homo sapiens	60-97