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. Mutations in AKT1 have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for AKT1
Clonality
Polyclonal
Formulation
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen
Host
Rabbit
Immunogen
Synthesized peptide derived from human Akt1 around the non-phosphorylation site of S129
Isotype
Rabbit IgG
Reactivity
Human, Mouse, Rat
Gene Id
207
Concentration
1 mg/ml
Purification
The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen
Storage Buffer
PBS containing 50% Glycerol, 0.5% BSA and 0.02% Sodium Azide