Background:

The serine-threonine protein kinase AKT1 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.

Alternative names:

AKT1; PKB; RAC; RAC-alpha serine/threonine-protein kinase; Protein kinase B; PKB; Protein kinase B alpha; PKB alpha; Proto-oncogene c-Akt; RAC-PK-alpha; AKT2; RAC-beta serine/threonine-protein kinase; Protein kinase Akt-2; Protein kinase B

Clonality:

Polyclonal

Reactivity:

Human,Mouse,Rat

Source:

Rabbit

Isotype:

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Immunogen:

Synthesized peptide derived from human Akt around the non-phosphorylation site of T308.

Concentration:

1mg/ml

Applications:

WB, IHC, ELISA

Recommende dilutions:

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Storage:

PBS with 0.02% sodium azide and 50% glycerol pH 7.4. Store at -20°C. Avoid repeated freeze-thaw cycles.

More info:

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Orders:

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