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Amiloride-sensitive sodium channel

Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Plays an essential role in electrolyte and blood pressure homeostasis, but also in airway surface liquid homeostasis, which is important for proper clearance of mucus. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception.

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Amiloride-sensitive sodium channel subunit alpha

Also known as Amiloride-sensitive sodium channel subunit alpha (Alpha-NaCH) (Epithelial Na(+) channel subunit alpha) (Alpha-ENaC) (ENaCA) (Nonvoltage-gated sodium channel 1 subunit alpha) (SCNEA).
ENaC-alpha: Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception. Probable heterotrimer containing one alpha, one beta and one gamma subunit. A delta subunit can replace the alpha subunit. Interacts with the WW domains of NEDD4, NEDD4L, WWP1 and WWP2. By aldosterone. Highly expressed in kidney and lung. Detected at intermediate levels in pancreas and liver, and at low levels in heart and placenta. Isoform 1 and isoform 2 predominate in all tissues. Expression of isoform 3, isoform 4 and isoform 5 is very low or not detectable, except in lung and heart. Activated by WNK1, WNK2, WNK3 and WNK4. Belongs to the amiloride-sensitive sodium channel (TC 1.A.6) family. SCNN1A subfamily. 6 isoforms of the human protein are produced by alternative splicing.

Protein type: Channel, sodium; Membrane protein, integral; Membrane protein, multi-pass; Transporter, ion channel

Chromosomal Location of Human Ortholog: 12p13

Cellular Component: apical plasma membrane; integral to plasma membrane; plasma membrane

Molecular Function: amiloride-sensitive sodium channel activity; protein binding; WW domain binding

Biological Process: multicellular organismal water homeostasis; sodium ion homeostasis

Disease: Bronchiectasis With Or Without Elevated Sweat Chloride 2; Pseudohypoaldosteronism, Type I, Autosomal Recessive

Amiloride-sensitive sodium channel subunit beta

Also known as Amiloride-sensitive sodium channel subunit beta (Beta-NaCH) (Epithelial Na(+) channel subunit beta) (Beta-ENaC) (ENaCB) (Nonvoltage-gated sodium channel 1 subunit beta) (SCNEB).
ENaC-beta: Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception. Defects in SCNN1B are a cause of autosomal recessive pseudohypoaldosteronism type 1 (AR-PHA1). PHA1 is a rare salt wasting disease resulting from target organ unresponsiveness to mineralocorticoids. There are 2 forms of PHA1: the autosomal recessive form that is severe, and the dominant form which is milder and due to defects in mineralocorticoid receptor. AR-PHA1 is characterized by an often fulminant presentation in the neonatal period with dehydration, hyponatraemia, hyperkalaemia, metabolic acidosis, failure to thrive and weight loss. The degree of channel function impairment differentially affects the renin-aldosterone system and urinary Na/K ratios, resulting in distinct genotype-phenotype relationships in PHA1 patients. Loss- of-function mutations are associated with a severe clinical course and age-dependent hyperactivation of the renin-aldosterone system. This feature is not observed in patients with missense mutations that reduce but do not eliminate channel function. Markedly reduced channel activity results in impaired linear growth and delayed puberty. Defects in SCNN1B are a cause of Liddle syndrome (LIDDS). It is an autosomal dominant disorder characterized by pseudoaldosteronism and hypertension associated with hypokalemic alkalosis. The disease is caused by constitutive activation of the renal epithelial sodium channel. Defects in SCNN1B are the cause of bronchiectasis with or without elevated sweat chloride type 1 (BESC1). A debilitating respiratory disease characterized by chronic, abnormal dilatation of the bronchi and other cystic fibrosis-like symptoms in the absence of known causes of bronchiectasis (cystic fibrosis, autoimmune diseases, ciliary dyskinesia, common variable immunodeficiency, foreign body obstruction). Clinical features include sub-normal lung function, sinopulmonary infections, chronic productive cough, excessive sputum production, and elevated sweat chloride in some cases. Belongs to the amiloride-sensitive sodium channel (TC 1.A.6) family. SCNN1B subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Channel, sodium; Membrane protein, integral; Membrane protein, multi-pass; Transporter, ion channel

Chromosomal Location of Human Ortholog: 16p12.2-p12.1

Cellular Component: integral to plasma membrane; plasma membrane

Molecular Function: amiloride-sensitive sodium channel activity; protein binding; WW domain binding

Biological Process: excretion; multicellular organismal water homeostasis; sodium ion homeostasis; sodium ion transport

Disease: Bronchiectasis With Or Without Elevated Sweat Chloride 1; Liddle Syndrome; Pseudohypoaldosteronism, Type I, Autosomal Recessive

Amiloride-sensitive sodium channel subunit beta-2

Also known as Amiloride-sensitive sodium channel subunit beta-2 (Beta-2-NaCH) (Epithelial Na(+) channel subunit beta-2) (Beta-2-ENaC) (Nonvoltage-gated sodium channel 1 subunit beta-2) (SCNEB2).
Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Plays an essential role in electrolyte and blood pressure homeostasis, but also in airway surface liquid homeostasis, which is important for proper clearance of mucus.

Amiloride-sensitive sodium channel subunit delta

Also known as Amiloride-sensitive sodium channel subunit delta (Delta-NaCH) (Epithelial Na(+) channel subunit delta) (Delta-ENaC) (ENaCD) (Nonvoltage-gated sodium channel 1 subunit delta) (SCNED).
ENaC-delta: Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception. Belongs to the amiloride-sensitive sodium channel (TC 1.A.6) family. SCNN1D subfamily. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Channel, sodium; Membrane protein, integral; Membrane protein, multi-pass; Transporter, ion channel

Chromosomal Location of Human Ortholog: 1p36.3-p36.2

Cellular Component: actin cytoskeleton; membrane; plasma membrane

Molecular Function: protein binding

Biological Process: sodium ion transport

Amiloride-sensitive sodium channel subunit gamma

Also known as Amiloride-sensitive sodium channel subunit gamma (Epithelial Na(+) channel subunit gamma) (ENaCG) (Gamma-ENaC) (Gamma-NaCH) (Nonvoltage-gated sodium channel 1 subunit gamma) (SCNEG).
ENaC-gamma: Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Controls the reabsorption of sodium in kidney, colon, lung and sweat glands. Also plays a role in taste perception. Defects in SCNN1G are a cause of Liddle syndrome (LIDDS). It is an autosomal dominant disorder characterized by pseudoaldosteronism and hypertension associated with hypokalemic alkalosis. The disease is caused by constitutive activation of the renal epithelial sodium channel. Defects in SCNN1G are the cause of bronchiectasis with or without elevated sweat chloride type 3 (BESC3). A debilitating respiratory disease characterized by chronic, abnormal dilatation of the bronchi and other cystic fibrosis-like symptoms in the absence of known causes of bronchiectasis (cystic fibrosis, autoimmune diseases, ciliary dyskinesia, common variable immunodeficiency, foreign body obstruction). Clinical features include sub-normal lung function, sinopulmonary infections, chronic productive cough, excessive sputum production, and elevated sweat chloride in some cases. Belongs to the amiloride-sensitive sodium channel (TC 1.A.6) family. SCNN1G subfamily.

Protein type: Channel, sodium; Membrane protein, integral; Membrane protein, multi-pass; Transporter, ion channel

Chromosomal Location of Human Ortholog: 16p12

Cellular Component: integral to plasma membrane; plasma membrane

Molecular Function: amiloride-sensitive sodium channel activity; ion channel activity; protein binding; sodium channel activity; WW domain binding

Biological Process: excretion; multicellular organismal water homeostasis; sodium ion homeostasis; sodium ion transport

Disease: Bronchiectasis With Or Without Elevated Sweat Chloride 3; Liddle Syndrome; Pseudohypoaldosteronism, Type I, Autosomal Recessive

Amiloride-sensitive sodium channel subunit gamma-2

Also known as Amiloride-sensitive sodium channel subunit gamma-2 (Epithelial Na(+) channel subunit gamma-2) (Gamma-2-ENaC) (Gamma-2-NaCH) (Nonvoltage-gated sodium channel 1 subunit gamma-2) (SCNEG2).
Sodium permeable non-voltage-sensitive ion channel inhibited by the diuretic amiloride. Mediates the electrodiffusion of the luminal sodium (and water, which follows osmotically) through the apical membrane of epithelial cells. Plays an essential role in electrolyte and blood pressure homeostasis, but also in airway surface liquid homeostasis, which is important for proper clearance of mucus.

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