SCNN1A antibody (AA 46-68)

Catalog No. ABIN863202

Product Details anti-SCNN1A Antibody

Target: SCNN1A (Sodium Channel, Nonvoltage-Gated 1 alpha (SCNN1A))

Binding Specificity: AA 46-68

Reactivity: Rat

Host: Rabbit

Clonality: Polyclonal

Conjugate: This SCNN1A antibody is un-conjugated

Application: Western Blotting (WB), Immunohistochemistry (IHC), Immunofluorescence (IF), Immunoprecipitation (IP), Immunocytochemistry (ICC)

Specificity: Detects ~85 kDa.

Cross-Reactivity: Human, Mouse, Rat, Xenopus laevis

Purification: Protein A Purified

Immunogen: Produced against a synthetic peptide mapping to the N-terminal of the alpha subunit (amino acids 46-68) of rat Alpha ENaC (antibody designation 3560-2).

Application Details

Application Notes:

• WB (1:1000)
• ICC/IF (1:400)
• IHC (1:25)
• optimal dilutions for assays should be determined by the user.

Comment:

1 μg/ml of ABIN863202 was sufficient for detection of alpha-ENaC in 35 μg of rat kidney tissue lysate by colorimetric immunoblot analysis using Goat anti-rabbit IgG:HRP as the secondary antibody.

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 1 mg/mL

Buffer: PBS, 50 % glycerol, 0.09 % sodium azide, Storage buffer may change when conjugated

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: -20 °C

Storage Comment: -20°C

References for anti-SCNN1A antibody (ABIN863202)

Khedr, Palygin, Pavlov, Blass, Levchenko, Alsheikh, Brands, El-Meanawy, Staruschenko: "Increased ENaC activity during kidney preservation in Wisconsin solution." in: BMC nephrology, Vol. 20, Issue 1, pp. 145, (2020) (PubMed).

Blass, Klemens, Brands, Palygin, Staruschenko: "Postprandial Effects on ENaC-Mediated Sodium Absorption." in: Scientific reports, Vol. 9, Issue 1, pp. 4296, (2019) (PubMed).

Pavlov, Levchenko, Ilatovskaya, Moreno, Staruschenko: "Renal sodium transport in renin-deficient Dahl salt-sensitive rats." in: Journal of the renin-angiotensin-aldosterone system : JRAAS, Vol. 17, Issue 3, (2017) (PubMed).

van Angelen, van der Kemp, Hoenderop, Bindels: "Increased expression of renal TRPM6 compensates for Mg(2+) wasting during furosemide treatment." in: Clinical kidney journal, Vol. 5, Issue 6, pp. 535-44, (2015) (PubMed).

Wen, Yuan, Warner, Wang, Cornelius, Wang-France, Li, Boettger, Sansom: "Increased Epithelial Sodium Channel Activity Contributes to Hypertension Caused by Na+-HCO3- Cotransporter Electrogenic 2 Deficiency." in: Hypertension, Vol. 66, Issue 1, pp. 68-74, (2015) (PubMed).

Zhang, Sun, Ding, Huang, Zhang, Jia: "Inhibition of Mitochondrial Complex-1 Prevents the Downregulation of NKCC2 and ENaCα in Obstructive Kidney Disease." in: Scientific reports, Vol. 5, pp. 12480, (2015) (PubMed).

Hye Khan, Pavlov, Christain, Neckář, Staruschenko, Gauthier, Capdevila, Falck, Campbell, Imig: "Epoxyeicosatrienoic acid analogue lowers blood pressure through vasodilation and sodium channel inhibition." in: Clinical science (London, England : 1979), Vol. 127, Issue 7, pp. 463-74, (2014) (PubMed).

Grahammer, Haenisch, Steinhardt, Sander, Roerden, Arnold, Cordts, Wanner, Reichardt, Kerjaschki, Ruegg, Hall, Moulin, Busch, Boerries, Walz, Artunc, Huber: "mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 111, Issue 27, pp. E2817-26, (2014) (PubMed).

Ramkumar, Stuart, Rees, Hoek, Sigmund, Kohan: "Collecting duct-specific knockout of renin attenuates angiotensin II-induced hypertension." in: American journal of physiology. Renal physiology, Vol. 307, Issue 8, pp. F931-8, (2014) (PubMed).

Pavlov, Levchenko, Staruschenko: "Role of Rho GDP dissociation inhibitor α in control of epithelial sodium channel (ENaC)-mediated sodium reabsorption." in: The Journal of biological chemistry, Vol. 289, Issue 41, pp. 28651-9, (2014) (PubMed).

Davies, Fraser, Galic, Choy, Katerelos, Gleich, Kemp, Mount, Power: "Novel mechanisms of Na+ retention in obesity: phosphorylation of NKCC2 and regulation of SPAK/OSR1 by AMPK." in: American journal of physiology. Renal physiology, Vol. 307, Issue 1, pp. F96-F106, (2014) (PubMed).

Jia, Liu, Sun, Kakizoe, Guan, Zhang, Zhou, Yang: "mPGES-1-derived PGE2 mediates dehydration natriuresis." in: American journal of physiology. Renal physiology, Vol. 304, Issue 2, pp. F214-21, (2013) (PubMed).

Roos, Bugaj, Mironova, Stockand, Ramkumar, Rees, Kohan: "Adenylyl cyclase VI mediates vasopressin-stimulated ENaC activity." in: Journal of the American Society of Nephrology : JASN, Vol. 24, Issue 2, pp. 218-27, (2013) (PubMed).

Pavlov, Ilatovskaya, Levchenko, Li, Ecelbarger, Staruschenko: "Regulation of ENaC in mice lacking renal insulin receptors in the collecting duct." in: FASEB journal : official publication of the Federation of American Societies for Experimental Biology, Vol. 27, Issue 7, pp. 2723-32, (2013) (PubMed).

Miller, Loewy: "ENaC γ-expressing astrocytes in the circumventricular organs, white matter, and ventral medullary surface: sites for Na+ regulation by glial cells." in: Journal of chemical neuroanatomy, Vol. 53, pp. 72-80, (2013) (PubMed).

Mamenko, Zaika, Prieto, Jensen, Doris, Navar, Pochynyuk: "Chronic angiotensin II infusion drives extensive aldosterone-independent epithelial Na+ channel activation." in: Hypertension, Vol. 62, Issue 6, pp. 1111-22, (2013) (PubMed).

van der Lubbe, Lim, Meima, van Veghel, Rosenbaek, Mutig, Danser, Fenton, Zietse, Hoorn: "Aldosterone does not require angiotensin II to activate NCC through a WNK4-SPAK-dependent pathway." in: Pflügers Archiv : European journal of physiology, Vol. 463, Issue 6, pp. 853-63, (2012) (PubMed).

Yu, Thelin, Rogers, Stutts, Randell, Grubb, Boucher: "Regional differences in rat conjunctival ion transport activities." in: American journal of physiology. Cell physiology, Vol. 303, Issue 7, pp. C767-80, (2012) (PubMed).

Edinger, Bertrand, Rondandino, Apodaca, Johnson, Butterworth: "The epithelial sodium channel (ENaC) establishes a trafficking vesicle pool responsible for its regulation." in: PLoS ONE, Vol. 7, Issue 9, pp. e46593, (2012) (PubMed).

Target Details for SCNN1A

Target: SCNN1A (Sodium Channel, Nonvoltage-Gated 1 alpha (SCNN1A))

Alternative Name: ENaC (SCNN1A Products)

Synonyms: BESC2 antibody, ENaCa antibody, ENaCalpha antibody, SCNEA antibody, SCNN1 antibody, ENaC antibody, Scnn1 antibody, mENaC antibody, SCNN1A antibody, alphaxENaC antibody, besc2 antibody, enaca antibody, scnn1 antibody, ENAC antibody, sodium channel epithelial 1 alpha subunit antibody, sodium channel, nonvoltage-gated 1 alpha antibody, sodium channel, non voltage gated 1 alpha subunit L homeolog antibody, Scnn1a antibody, SCNN1A antibody, scnn1a.L antibody

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, α, β, and γ. 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).

Gene ID: 25122

NCBI Accession: NP_113736

UniProt: Q6IRJ1