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Validated All-in-One™ qPCR Primer for ATP1B1(NM_001677.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The protein encoded by this gene belongs to the family of Na+/K+ and H+/K+ ATPases beta chain proteins, and to the subfamily of Na+/K+ -ATPases. Na+/K+ -ATPase is an integral membrane protein responsible for establishing and maintaining the electrochemical gradients of Na and K ions across the plasma membrane. These gradients are essential for osmoregulation, for sodium-coupled transport of a variety of organic and inorganic molecules, and for electrical excitability of nerve and muscle. This enzyme is composed of two subunits, a large catalytic subunit (alpha) and a smaller glycoprotein subunit (beta). The beta subunit regulates, through assembly of alpha/beta heterodimers, the number of sodium pumps transported to the plasma membrane. The glycoprotein subunit of Na+/K+ -ATPase is encoded by multiple genes. This gene encodes a beta 1 subunit. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq].
Gene References into function
- Carboxy-terminus of HKalpha(2) facilitates proper folding of tHKalpha(2)/beta(1) complex allowing translocation of heterodimer to plasma membrane where potassium uptake occurs. Otherwise, alpha/beta complex is destined for degradation.
- N-glycans linked to the beta2 subunit of the Na,K-ATPase contain apical sorting information, and the high abundance of the beta2 subunit isoform along with the absence of the beta1 subunit, is responsible for the unusual apical location of the Na,K-ATPas
- Data show that deglycosylation in polarized hepatic cells by drugs, or by site-directed mutagenesis of the N-linked-glycosylation residues, cause the Na+/K+-ATPase beta-subunit to traffic from the native basolateral to the apical/canalicular domain.
- these studies are indicative of a synergism between Sp1 and CREB in mediating regulation of Na-K ATPase beta1 subunit by PGRE3; while regulation occurring through PGRE1 also involves Sp1 and CREB.
- Study identifies an interaction between Wolframin and Na+/K+ ATPase beta1 subunit in transfected Cos7 cells, and between endogenous proteins in placental, neuroblastoma and MIN6 pancreatic beta-cell lines.
- E2A and Na/K-ATPase beta1 subunit expression in epithelial cells are regulated by interactions between these proteins.
