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v-akt murine thymoma viral oncogene homolog 1

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NCBI Description of AKT1

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.

Community Annotation of AKT1 Add / Edit AKT1: Annotations

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Figure notes


• "Mouse over" a mutation to see details.
• Missense green saturation indicates evolutionary conservation of the mutated positions.
• Red hashes in protein strip are splice sites.
• Blue-white-red bars are log2 copy ratio distributions (–1 to +1) from Zack et al. (2013).


Legend

AKT1 is highly significantly mutated in
Breast
BRCA
19 patients (2%)
combined cohort
PanCan
40 patients (0%)
AKT1 is significantly mutated in
Endometrial
UCEC
8 patients (3%)
AKT1 is near significance in

Click on a tumor type to see its full list of significant genes.

Data details


Mutation list for AKT1