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. 2022 Oct 3;13(10):846. doi: 10.1038/s41419-022-05250-5

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — A A traditional perspective of AKT activation assumes that PI3K, which converts PM-associated PIP2 to PIP3 in response to Growth Factors (GF) and other stimuli, leads to PIP3-mediated recruitment of cytosolic AKT to PM. The conformational change elicited by AKT PH domain binding to PIP3 allows phosphorylation of AKT by PDK1 and mTORC2. As a result, activated AKT concertedly regulates a great variety of targets and functions in the cytosol and the nucleus, among other subcellular compartments. B Examples of physiological and pathological processes in which AKT is implicated. C Key steps of viral infection regulated by AKT.