SCNN1A antibody (AA 629-650)
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- Target See all SCNN1A Antibodies
- SCNN1A (Sodium Channel, Nonvoltage-Gated 1 alpha (SCNN1A))
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Binding Specificity
- AA 629-650
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Reactivity
- Rat
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Host
- Rabbit
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Clonality
- Polyclonal
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Conjugate
- This SCNN1A antibody is un-conjugated
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Application
- Western Blotting (WB), Immunohistochemistry (IHC), Immunofluorescence (IF), Immunocytochemistry (ICC)
- Specificity
- Detects ~83 kDa.
- Cross-Reactivity
- Hamster, Human, Mouse, Rat, Xenopus laevis
- Purification
- Protein A Purified
- Immunogen
- Produced against the C-terminal tail (amino acids 629-650) of rat gamma ENaC (antibody designation L550)
- Top Product
- Discover our top product SCNN1A Primary Antibody
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- Application Notes
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- WB (1:1000)
- IHC (1:100)
- optimal dilutions for assays should be determined by the user.
- Comment
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1 μg/ml of ABIN863204 was sufficient for detection of gamma-ENaC in 20 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
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- 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
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Increased ENaC activity during kidney preservation in Wisconsin solution." in: BMC nephrology, Vol. 20, Issue 1, pp. 145, (2020) (PubMed).
: "Postprandial Effects on ENaC-Mediated Sodium Absorption." in: Scientific reports, Vol. 9, Issue 1, pp. 4296, (2019) (PubMed).
: "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).
: "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).
: "Prostasin interacts with the epithelial Na+ channel and facilitates cleavage of the γ-subunit by a second protease." in: American journal of physiology. Renal physiology, Vol. 307, Issue 9, pp. F1080-7, (2014) (PubMed).
: "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).
: "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).
: "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).
: "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).
: "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).
: "Intersubunit conformational changes mediate epithelial sodium channel gating." in: The Journal of general physiology, Vol. 144, Issue 4, pp. 337-48, (2014) (PubMed).
: "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).
: "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).
: "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).
: "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).
: "Regional differences in rat conjunctival ion transport activities." in: American journal of physiology. Cell physiology, Vol. 303, Issue 7, pp. C767-80, (2012) (PubMed).
: "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).
: "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).
: "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).
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Increased ENaC activity during kidney preservation in Wisconsin solution." in: BMC nephrology, Vol. 20, Issue 1, pp. 145, (2020) (PubMed).
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- Target
- SCNN1A (Sodium Channel, Nonvoltage-Gated 1 alpha (SCNN1A))
- Alternative Name
- ENaC (SCNN1A Products)
- 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
- 24768
- NCBI Accession
- NP_058742
- UniProt
- P37091
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