*Optimal dilutions/concentrations should be determined by the researcher.
Not tested in other applications.
PC-12 , Rat2 , MCF-7 , MCF-7(500 nM PMA treatment for 1 hr) , MCF-7(500 nM PMA treatment for 2 hr) , MCF-7(500 nM PMA treatment for 4 hr) , MCF-7(500 nM PMA treatment for 6 hr) , HUVEC , HUVEC (5 ng/ml VEGF treatment for 10 min) , NIH-3T3 , NIH-3T3 (starvation for 16 hr and 5 ng/ml PDGF treatment for 15 min)
This antibody is raised against human AKT1 phosphorylated at Ser473. Based on sequence homology, it is predicted to react with AKT2 and AKT3 when phosphorylated at the corresponding residues - AKT2 Ser474 and AKT3 Ser472.
Zebrafish, Sheep, Cat, Chicken, Pig, Xenopus laevis, Rhesus Monkey(>80% identity)
1XPBS, 1% BSA, 20% Glycerol (pH7). 0.025% ProClin 300 was added as a preservative.
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
0.06 mg/ml (Please refer to the vial label for the specific concentration.)
Carrier-protein conjugated synthetic peptide corresponding to residues around human AKT (phospho Ser473/474/472). The exact sequence is proprietary.
Purified by antigen-affinity chromatography.
For laboratory use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Akt Serine/Threonine Kinase 1,Akt,Cws6,Pkb,Pkb-Alpha,Prkba,Rac,Rac-Alpha,Akt1
Cytoplasm , Nucleus , Cell membrane
The serine-threonine protein kinase encoded by the AKT1 gene is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq]