title: Akt signaling: a damaging interaction makes good.
abstract: Phosphorylation of the protein kinase Akt at Ser473 is a key regulatory event in the induction of cellular survival mechanisms. A new study provides a novel mechanism for Akt activation. In cells and mice exposed to DNA-damaging insults, Ser473 phosphorylation is mediated by the DNA-dependent protein kinase at sites of DNA double-strand breaks. This event triggers the induction of a transcriptional program that promotes survival in response to DNA damage.
authors.affiliation: Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. atoker@bidmc.harvard.edu
authors.forename: Alex
authors.initials: A
authors.lastname: Toker
mesh_terms: D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000737:chemistry / Q000378:metabolism*; D012694:Serine / Q000378:metabolism
chemical_list: D012694:Serine; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt