Akt phosphorylates insulin receptor substrate to engage negative feedback and limit signal propagation.

Cavin-3 is a tumor suppressor protein that inhibits Akt signaling, suppresses Warburg metabolism, promotes apoptosis, and protects against cachexia.

Interleukin 4 signaling co-opts the Akt-mTORC1-Acly pathway to couple metabolic input to the control of energetically demanding processes during macrophage M2 activation.

Information transduction capacity of mammalian cells is high and varies substantially from cell to cell.

Akt activation is required for neural crest differentiation through regulation of Sox10 activity.

Age-dependent changes in DNA methylation are tightly coupled to the metabolic state, and is partly under genetic regulation, and longer lifespan is associated with lower epigenetic entropy at CpGs that increase in methylation with age.

Human yolk sac-like cells, which share characteristics with the post-implantation human hypoblast, can model the interaction between the epiblast and hypoblast that occurs during early human development.

A signalling cascade involving PI3K/Akt1 remodels the extra-cellular matrix to achieve atypical cellular responses and control cell fate specification within the embryonic endoderm.

The kinase AKT acts as a nodal point that coordinates both positive and negative cues to regulate the regeneration of central nervous system axons in adult mice.

Akt can regulate the ubiquitin-proteasome system by mediating phosphorylation and activation of USP14, which may have implications in the control of global proteostasis by growth factors and in tumorigenesis.