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NSJ Bioreagents

SKU:F50140-0.08ML

Anti-AKT Antibody

Anti-AKT Antibody

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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.

Specifications

Family Primary antibody
Formulation In 1X PBS, pH 7.4, with 0.09% sodium azide
Format Purified
Host Animal Rabbit
Clonality Polyclonal (rabbit origin)
Isotype Rabbit Ig
Species Reactivity Human
Predicted Species Reactivity Bovine, Mouse, Rat
Application WB, IF, FACS, ELISA
Application Details Western blot: 1:1000,Immunofluorescence: 1:10-1:50,Flow Cytometry: 1:10-1:50
Application Note Titration of the anti-AKT antibody may be required due to differences in protocols and secondary/substrate sensitivity.
Immunogen A portion of amino acids 49-76 from human AKT1 was used as the immunogen for this anti-AKT antibody.
Purity Purified
Storage Aliquot the anti-AKT antibody and store frozen at -20oC or colder. Avoid repeated freeze-thaw cycles.
Limitation This anti-AKT antibody is available for research use only.
Uniprot # P31749
Status Available
PDF Link https://www.nsjbio.com/tds-pdf/anti-akt-antibody-f50140
Title Anti-AKT Antibody
Description 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.
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