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 this gene have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for this gene.
Dilutions
WB 1:500 - 1:2000 IF 1:50 - 1:200
Format
Calculated MW
48kDa/55kDa
Observed MW
60kDa
Immunogen
A synthetic phosphorylated peptide around T308 of human AKT1 (NP_005154.2).
Modification
Phospho T308
Storage
-20°C
Images
Western blot analysis of extracts of HeLa cells, using Phospho-AKT1-T308 antibody (144-50304) at 1:2000 dilution. HeLa cells were treated by 10% FBS for after serum-starvation overnight. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% BSA. Detection: ECL Enhanced Kit. Exposure time: 90s.
Immunofluorescence analysis of HeLa cells using Phospho-AKT1-T308 antibody (144-50304) at dilution of 1:100. Blue: DAPI for nuclear staining.
Expiration:
12 months from the date of shipment when stored properly.
