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Key Documents

06-520

Sigma-Aldrich

Anti-Na+/K+ ATPase α-1 Antibody

Upstate®, from rabbit

Synonym(s):

Anti-CMT2DD

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

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

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
Research Sub Category
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.

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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Magnesium depletion enhances cisplatin-induced nephrotoxicity.
H Lajer, M Kristensen, H H Hansen, S Nielsen, J Fr?kiaer, L F Ostergaard, S Christensen et al.
Cancer Chemotherapy and Pharmacology null
J H Dominguez et al.
The Journal of clinical investigation, 98(2), 395-404 (1996-07-15)
Injury to the renal proximal tubule is common and may be followed by either recovery or cell death. The survival of injured cells is supported by a transient change in cellular metabolism that maintains life even when oxygen tension is
Purification of active Na+-K+-ATPase using a new ouabain-affinity column
Yingst, D. R., et al
The American Journal of Physiology, 275, C1167-C1177 (1998)
Intrarenal octreotide treatment prevents sodium retention in liver cirrhotic rats: evidence for direct effects within the thick ascending limb of Henle's loop.
Jonassen, TE; Christensen, S; Marcussen, N; Petersen, JS
American Journal of Physiology: Renal Physiology null
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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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