SCNN1A Antikörper (AA 617-638)

Produktnummer ABIN863203

Produktdetails anti-SCNN1A Antikörper

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

Bindungsspezifität: AA 617-638

Reaktivität: Ratte

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser SCNN1A Antikörper ist unkonjugiert

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

Spezifität: Detects ~87 kDa.

Kreuzreaktivität: Hamster, Human, Maus, Ratte, Xenopus laevis

Aufreinigung: Protein A Purified

Immunogen: Produced against the C-terminal tail (amino acids 617-638) of rat beta ENaC (antibody designation 3755-2)

Anwendungsinformationen

Applikationshinweise:

• WB (1:1000)
• IHC (1:100)
• optimal dilutions for assays should be determined by the user.

Kommentare:

1 μg/ml of ABIN863203 was sufficient for detection of beta-ENaC in 20 μg of rat kidney tissue lysate by colorimetric immunoblot analysis using Goat anti-rabbit IgG:HRP as the secondary antibody.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 1 mg/mL

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

Konservierungsmittel: Sodium azide

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

Lagerung: -20 °C

Informationen zur Lagerung: -20°C

Referenzen für anti-SCNN1A Antikörper (ABIN863203)

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).

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).

Vitzthum, Seniuk, Schulte, Müller, Hetz, Ehmke: "Functional coupling of renal K+ and Na+ handling causes high blood pressure in Na+ replete mice." in: The Journal of physiology, Vol. 592, Issue Pt 5, pp. 1139-57, (2014) (PubMed).

Collier, Tomkovicz, Peterson, Benson, Snyder: "Intersubunit conformational changes mediate epithelial sodium channel gating." in: The Journal of general physiology, Vol. 144, Issue 4, pp. 337-48, (2014) (PubMed).

Xu, Barone, Brooks, Soleimani: "Double knockout of carbonic anhydrase II (CAII) and Na(+)-Cl(-) cotransporter (NCC) causes salt wasting and volume depletion." in: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, Vol. 32, Issue 7, pp. 173-83, (2014) (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).

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).

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).

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).

Soleimani, Barone, Xu, Shull, Siddiqui, Zahedi, Amlal: "Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 109, Issue 33, pp. 13368-73, (2012) (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).

Ilatovskaya, Pavlov, Levchenko, Negulyaev, Staruschenko: "Cortical actin binding protein cortactin mediates ENaC activity via Arp2/3 complex." in: FASEB journal : official publication of the Federation of American Societies for Experimental Biology, Vol. 25, Issue 8, pp. 2688-99, (2011) (PubMed).

Details zu SCNN1A

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

Andere Bezeichnung: ENaC (SCNN1A Produkte)

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

Hintergrund: 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).

Gen-ID: 24767

NCBI Accession: NP_036780

UniProt: P37090