Novel HIF2A mutations disrupt oxygen sensing, leading to polycythemia, paragangliomas, and somatostatinomas Blood, Mar 2013; 121: 2563 - 2566.
[anti-HA]
Regulation of the PI3-K/Akt Survival Pathway in the Rat Endometrium Biol Reprod, Mar 2013; 88: 79.
[Akt3]
RNA elements directing in vivo assembly of the 7SK/MePCE/Larp7 transcriptional regulatory snRNP Nucleic Acids Res., Mar 2013; 10.1093/nar/gkt159.
[LA]
Ruxolitinib as potential targeted therapy for patients with JAK2 rearrangements Haematologica, Mar 2013; 98: 404 - 408.
[JAK2]
A phospho specific peptide corresponding to residues surrounding Tyrosine 10 of human Na+/K+ATPase a was used as an immunogen. This antibody only detects Na+/K+ATPase a phosphorylated at Tyrosine 10.
Buffer
Store at -20 °C. Buffer: Antibody buffer, sodium azide, glycerol, and BSA. Stable for 12 months from date of receipt.
Na+, K+-ATPase is a heterodimeric enzyme responsible for the active maintenance of sodium and potassium gradients across the plasma membrane (1). The sodium- and potassium-dependent adenosine triphosphatase (Na+,K(+)-ATPase) maintains the transmembrane Na+ gradient to which is coupled all active cellular transport systems (2). It is well accepted that inhibition of the Na,K-ATPase in the heart, through effects on the Na/Ca exchanger, raises the intracellular Ca2+ concentration and strengthens cardiac contraction. Assessing the phenotypes of mouse hearts with genetically reduced levels of Na,K-ATPase alpha 1 or alpha 2 isoforms clearly demonstrates different functional roles for these isoforms in vivo. Results definitively illustrate a specific role for the alpha 2 Na,K-ATPase isoform in Ca2+ signaling during cardiac contraction (3).
Related Pathway
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Western blot analysis on HeLa cell lysates using anti-Phospho-Na+/K+ATPase ? (pY10) RabMAb. Cells were either (A) untreated (B) treated with Pervanadate.
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