antibody

ENaC Gamma Antibody: ATTO 655

MBS806112

0.1 mg

450 USD

polyclonal

rabbit

ATTO 655

mouse, rat

western blot, immunohistochemistry, immunocytochemistry

Antibody

ENaC Gamma Antibody: ATTO 655

ENaC Gamma

Scnn1g

amiloride-sensitive sodium channel subunit gamma; Amiloride-sensitive sodium channel subunit gamma; amiloride-sensitive sodium channel subunit gamma; SCNEG; gamma-ENaC; gamma-NaCH; epithelial Na(+) channel subunit gamma; epithelial sodium channel gamma subunit; nonvoltage-gated sodium channel 1 subunit gamma; sodium channel, nonvoltage-gated, type I, gamma; amiloride sensitive sodium channel gamma1 subunit; Sodium channel nonvoltage-gated 1 gamma (epithelial); Sodium channel, nonvoltage-gated 1, gamma (epithelial); sodium channel, non-voltage-gated 1, gamma subunit; Epithelial Na(+) channel subunit gamma; Gamma-ENaC; Gamma-NaCH; Nonvoltage-gated sodium channel 1 subunit gamma; SCNEG

Scnn1g; Scnn1g; ENaC; Gamma-ENaC

SCNNG_RAT

Polyclonal

Rabbit

Rat, Mouse

650

Affinity Purified

1mg/mL

-20 degree C

Western Blot (WB), Immunohistochemistry (IHC), Immunofluorescence (IF); Immunocytochemistry (ICC)

WB: (1:1000. optimal dilutions for assays should be determined by the user.

Conjugate: ATTO 655. Immunogen: Produced against the C-terminal tail (amino acids 629-650) of rat gamma ENaC (antibody designation L550)

Storage Buffer: PBS, 50% glycerol, 0.09% sodium azide. Cellular Localization: Apical Cell Membrane. Gene ID: 24768. Accession Number: NP _058742. Swiss Prot: P37091

Ion Channels, Transporters

Background Info: Detects ~83kDa. Scientific Background: The Epithelial Sodium Channel (ENaC) is a membrane ion channel permeable to Na+ ions. It is located in the apical plasma membrane of epithelia in the kidneys, lung, colon, and other tissues where it plays a role in trans epithelial Na+-ion transport (1). Specifically Na+ transport via ENaC occurs across many epithelial surfaces, and plays a key role in regulating salt and water absorption (2). ENaCs are composed of three structurally related subunits that form a tetrameric channel, alpha, beta, and gamma. The expression of its alpha and beta subunits is enhanced as keratinocytes differentiate (3, 4). The beta and gamma-ENaC subunits are essential for edema fluid to exert its maximal effect on net fluid absorption by distal lung epithelia(5). And it has been concluded that the subunits are differentially expressed in the retina of mice with ocular hypertension, therefore the up-regulation of alpha-ENaC proteins could serve as a protection mechanism against elevated intraocular pressure (6).

1. Kakizoe Y., et al. (2009) J Hpyertens. 27(8): 1679-1689. 2. Gu Y. (2008) J Cell Physiol. 216(2):453-457. 3. Bruns J.B. (2003) Am J Physiol Renal Physiol. 285(4): F600-F609. 4. Mauro T., et al. (2002) J Invest Dermatol. 118(4): 589-594. 5. Elias N., et al. (2007) Am J Physiol Lung Cell Mol Physiol. 293(3): L537-45. 6. Dyka F.M., May C.A. and Enz R. (2005) J Neurochem. 94(1): 120-128. 1. Ilatovskaya, D.V., Pavlov, T.S., Levchenko, V., Negulyaev, Y.A. and Staruschenko, A. (2011). Cortical actin binding protein cortactin mediates ENaC activity via Arp2/3 complex. The FASEB Journal. 25 (8), 2688-2699. doi: 10.1096/fj.10-167262. 2. Edinger, R.S. et al. (2012). The Epithelial Sodium Channel (ENaC) Establishes a Trafficking Vesicle Pool Responsible for Its Regulation. PLoS ONE. 7(9): e46593. doi: 10.1371/journal.pone.0046593. 3. van der Lubbe, N. et al. (2012). Aldosterone does not require angiotensin II to activate NCC through a WNK4 SPAK dependent pathway. Euro J Physiol. 463 (6), 853-863. doi:10.1007/s00424-012-1104-0.

25742790

NP_058742

NM_017046.1

P37091

Aldosterone-regulated Sodium Reabsorption Pathway (130622); Aldosterone-regulated Sodium Reabsorption Pathway (130590); Taste Transduction Pathway (83480); Taste Transduction Pathway (499)

acts as an epithelial sodium ion channel; regulates salt and fluid transport in the kidney [RGD, Feb 2006]

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: Transporter, ion channel; Membrane protein, multi-pass; Membrane protein, integral; Channel, sodium. Cellular Component: cell surface; membrane; integral to plasma membrane; apical plasma membrane; integral to membrane; external side of plasma membrane. Molecular Function: amiloride-sensitive sodium channel activity; protein binding; WW domain binding; sodium channel activity. Biological Process: sensory perception of taste; sodium ion transport; response to hypoxia; sodium ion homeostasis; multicellular organismal water homeostasis; wound healing, spreading of epidermal cells

0.1 mg

450 USD