title: AKT signaling in physiology and disease.
abstract: The serine/threonine kinase AKT functions as a critical mediator of signaling downstream of PI3 kinase. Studies over the last two decades have firmly established the importance of AKT in the regulation of cell survival, proliferation, and insulin-dependent metabolic cell responses. AKT executes these diverse tasks through phosphorylation of numerous cellular substrates. Substantial progress has been made in understanding the regulation of AKT activity by upstream kinases and elucidating downstream mechanisms that mediate its myriad cellular effects. Here, we present an overview of AKT regulation and function in physiological and pathological settings. An emphasis is placed on the involvement of aberrant AKT signaling in human diseases ranging from diabetes to cancer and neurological diseases.
authors.affiliation: Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
authors.forename: Krishna M
authors.initials: KM
authors.lastname: Vasudevan
authors.forename: Levi A
authors.initials: LA
authors.lastname: Garraway
mesh_terms: D000818:Animals; D017209:Apoptosis; D004789:Enzyme Activation; D005947:Glucose / Q000378:metabolism; D006801:Humans; D009369:Neoplasms / Q000209:etiology; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
chemical_list: D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D005947:Glucose