Rabbit anti-Mouse, Rat ENaC Beta Polyclonal Antibody | anti-Scnn1b antibody

ENaC Beta Antibody: Alkaline Phosphatase

Cat. Num. AAA805399

• Gene Names: Scnn1b; RNENACB
• Reactivity: Mouse, Rat
• Applications: Western Blot, Immunohistochemistry, Immunoprecipitation, Immunofluorescence
• Synonyms: ENaC Beta; Polyclonal Antibody; ENaC Beta Antibody: Alkaline Phosphatase; Scnn1b; anti-Scnn1b antibody

• Host: Rabbit
• Reactivity: Mouse, Rat
• Clonality: Polyclonal
• Form/Format: Affinity Purified
• Concentration: 1mg/mL (varies by lot)
• Sequence Length: 638

• Applicable Applications for anti-Scnn1b antibody: Western (WB), Immunohistochemistry (IHC), Immunoprecipitation (IP), Immunofluorescence (IF)
• Application Notes: 1:1000 (WB)
• Conjugate: Alkaline Phosphatase
• Storage Buffer: PBS, 50% glycerol, 0.09% sodium azide.
• Preparation and Storage: -20 degree C

Immunohistochemistry (IHC)

(Immunohistochemistry analysis using Rabbit Anti-ENaC Polyclonal Antibody (SPC-404). Tissue: kidney tissue. Species: Rat. Primary Antibody: Rabbit Anti-ENaC Polyclonal Antibody (SPC-404) at 1:100. Secondary Antibody: FITC Goat Anti-Rabbit (green).)

Western Blot (WB)

(Western blot analysis of Rat kidney tissue lysates showing detection of ENaC protein using Rabbit Anti-ENaC Polyclonal Antibody (SPC-404). Primary Antibody: Rabbit Anti-ENaC Polyclonal Antibody (SPC-404) at 1:1000.)

Western Blot (WB)

(Western blot analysis of Mouse mpkCCD cell lysates showing detection of ENaC protein using Rabbit Anti-ENaC Polyclonal Antibody (SPC-404). Primary Antibody: Rabbit Anti-ENaC Polyclonal Antibody (SPC-404) at 1:1000.)

Western Blot (WB)

(Western blot analysis of Mouse kidney cortex showing detection of ENaC protein using Rabbit Anti-ENaC Polyclonal Antibody (SPC-404). Primary Antibody: Rabbit Anti-ENaC Polyclonal Antibody (SPC-404) at 1:1000. Low-salt diet (lanes 1-4) compared to a high-salt diet (lanes 5-8).)

Related Product Information for anti-Scnn1b antibody

Background Info: Detects ~87kDa.

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).

Product Categories/Family for anti-Scnn1b antibody

Ion Channels; Transporters

References

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

NCBI and Uniprot Product Information

• NCBI GI #: 25742736
• NCBI GeneID: 24767
• NCBI Accession #: NP_036780
• NCBI GenBank Nucleotide #: NM_012648.1
• UniProt Accession #: P37090; O09183
• Molecular Weight: 71,995 Da
• NCBI Official Full Name: amiloride-sensitive sodium channel subunit beta
• NCBI Official Synonym Full Names: sodium channel, non-voltage-gated 1, beta subunit
• NCBI Official Symbol: Scnn1b
• NCBI Official Synonym Symbols: RNENACB
• NCBI Protein Information: amiloride-sensitive sodium channel subunit beta; SCNEB; beta-ENaC; beta-NaCH; epithelial Na(+) channel subunit beta; sodium channel, nonvoltage-gated 1, beta; nonvoltage-gated sodium channel 1 subunit beta; sodium channel, nonvoltage-gated, type I, beta
• UniProt Protein Name: Amiloride-sensitive sodium channel subunit beta
• Protein Family: Amiloride-sensitive sodium channel
• UniProt Gene Name: Scnn1b
• UniProt Synonym Gene Names: Beta-ENaC
• UniProt Entry Name: SCNNB_RAT

NCBI Description

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

Uniprot Description

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; Transporter, ion channel; Membrane protein, multi-pass

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; regulation of sodium ion transport; multicellular organismal water homeostasis; wound healing, spreading of epidermal cells