Western Blot: epithelial Sodium Channel alpha Antibody [NB100-74357] - Analysis of 25 ug of Daudi (lane 1) and mouse brain (lane 2) cell lysates onto an SDS polyacrylamide gel.
Immunocytochemistry/ Immunofluorescence: epithelial Sodium Channel alpha Antibody [NB100-74357] - performed using 70% confluent log phase HEK-293 cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, ...read more
Immunocytochemistry/ Immunofluorescence: epithelial Sodium Channel alpha Antibody [NB100-74357] - performed using 70% confluent log phase HEK 293 cells. The cells were fixed with 4% paraformaldehyde for 10 minutes, ...read more
ICC/IF uage was reported in scientific literature (PMID: 25953733). WB: Specifically detects an approx. 97 kDa protein representing glycosylated alpha-ENaC from NIH-3T3 cells, and an approx. 75 kDa protein representing the unglycosylated alpha-ENaC protein from human brain samples.
76 kDa. Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.
Read Publications using NB100-74357 in the following applications:
Epithelial Sodium Channel alpha (SCNN1A) is a subunit of the epithelial sodium channel (ENaC). ENac has high sodium selectivity, low conductance, and amiloride sensitivity. The functional channel of ENaC is composed of at least 3 subunits, alpha (SCNN1A), beta (SCNN1B), and gamma (SCNN1G). The 3 subunits show sequence similarities to one another, indicating descent from a common ancestral gene. Each encodes a protein containing 2 transmembrane domains, with intracellular amino and carboxyl termini. The alpha subunit supports sodium conductance when expressed alone; the beta and gamma subunits do not support sodium conductance by themselves, but greatly augment the channel activity when expressed in conjunction with the alpha subunit. ENaC in the kidney, lung and colon plays an essential role in trans- epithelial sodium and fluid balance. ENaC also mediates aldosterone-dependent sodium re-uptake in the distal nephron of the kidney, thus regulating blood pressure. Gain-of-function mutations in beta- or gamma-ENaC can cause severe arterial hypertension (Liddel's syndrome) and loss-of-function mutations in alpha- or beta-ENaC causes pseudohypoaldosteronism (PHA-1).
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
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