06-520
Anti-Na+/K+ ATPase α-1 Antibody
Upstate®, from rabbit
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biological source
rabbit
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
polyclonal
species reactivity
bovine, rat, human
packaging
antibody small pack of 25 μg
manufacturer/tradename
Upstate®
technique(s)
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
ambient
target post-translational modification
unmodified
Gene Information
rat ... Atp1A1(24211)
Related Categories
General description
Na+/K+ ATPase α-1 is a human gene and functions to maintain Na+ and K+ across the cell membrane which is important for osmoregulation. It is a component of (Na+/K+) ATPase, a transporter that catalyzes the hydrolysis of ATP and transports sodium and potassium ions across the plasma membrane. It also partners with Src and other signaling proteins. Binding of ouabain and other cardiotonic steroids to the (Na+/K+) ATPase activates Src, resulting in the assembly and activation of multiple signaling cascades. Binding of ouabain also induces a positive inotropic effect. Diseases associated with ATPase are Thyrotoxic periodic paralysis and hyperthyroidism. (References: Wikipedia and http://www.bioportfolio.com/gene/476-ATP1A1.html)
Specificity
Expected to cross-react with Rat-100%, Mouse-99%; human, pig, rabbit, monkey-96%.
Recognizes the α-1 subunit isoform of Na+/K+ ATPase.
Immunogen
Epitope: Cytoplasmic domain
GST-tagged ATPase.
Application
Research Category
Neuroscience
Neuroscience
Research Sub Category
Ion Channels & Transporters
Ion Channels & Transporters
This Anti-Na+/K+ ATPase α-1 Antibody is validated for use in IC, IP, WB for the detection of Na+/K+ ATPase α-1.
Quality
Routinely evaluated by Immunoprecipitation on rat brain microsomal prep. lysate.
Target description
112 kDa
Physical form
Format: Purified
Protein A purified
Purified antibody in buffer containing 0.1M Tris-Glycine (pH7.4) 150mM NaCl and 0.05% NaN3.
Storage and Stability
Stable for 1 year at 2-8ºC from date of receipt.
Analysis Note
Control
Rat Brain Microsomal Prep. lysate.
Rat Brain Microsomal Prep. lysate.
Other Notes
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Biochimica et biophysica acta, 1850(6), 1286-1296 (2015-03-07)
Band keratopathy, an ocular disease that is characterized by hypercalcemia and opaque bands across the cornea, has been associated with kidney disease. Type-II renal tubular acidosis (RTA), a condition in which the kidneys fail to recover bicarbonate (HCO3-) in the
Antisera specific for the alpha 1, alpha 2, alpha 3, and beta subunits of the Na,K-ATPase: differential expression of alpha and beta subunits in rat tissue membranes.
Biochemistry, 28, 4531-4535 (1989)
Insulin-induced recruitment of glucose transporter 4 (GLUT4) and GLUT1 in isolated rat cardiac myocytes. Evidence of the existence of different intracellular GLUT4 vesicle populations
The Journal of Biological Chemistry, 272, 7085-7092 (1997)
Purification and characterization of (Na+ plus K+ )-ATPase. 3. Purification from the outer medulla of mammalian kidney after selective removal of membrane components by sodium dodecylsulphate.
Biochimica et Biophysica Acta, 356, 36-52 (1974)
Scientific reports, 5, 18420-18420 (2015-12-18)
Excessive exposure to club drug (GHB) would cause cognitive dysfunction in which impaired hippocampal Ca(2+)-mediated neuroplasticity may correlate with this deficiency. However, the potential changes of in vivo Ca(2+) together with molecular machinery engaged in GHB-induced cognitive dysfunction has never
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