For reference only. Please follow the manual included in your kit for instructions.
Catalog Number
RD90296A
Western blot analysis of extracts from wild type(WT) and AKT1 knockout (KO) HeLa cells, using AKT1 Polyclonal Antibody at 1:1000 dilution.
Immunohistochemistry of paraffin-embedded human liver cancer using AKT1 Polyclonal Antibody at dilution of 1:100 (40x lens).Perform microwave antigen retrieval with 10 mM PBS buffer pH 7.2 before commencing with IHC staining protocol.
Immunohistochemistry of paraffin-embedded human esophageal using AKT1 Polyclonal Antibody at dilution of 1:100 (40x lens).Perform microwave antigen retrieval with 10 mM PBS buffer pH 7.2 before commencing with IHC staining protocol.
Immunofluorescence analysis of NIH/3T3 cells using [KO Validated] AKT1 Polyclonal Antibody at dilution of 1:50 (40x lens). Blue: DAPI for nuclear staining.
Immunofluorescence analysis of PC-12 cells using [KO Validated] AKT1 Polyclonal Antibody at dilution of 1:50 (40x lens). Blue: DAPI for nuclear staining.
Immunofluorescence analysis of U2OS cells using [KO Validated] AKT1 Polyclonal Antibody at dilution of 1:50 (40x lens). Blue: DAPI for nuclear staining.
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.