title: Regulation of Ras signaling by the cell cycle.
abstract: It is well known that upregulation of Ras activity can promote cell-cycle progression. Now recent studies indicate that a reciprocal relationship also exists; that is, the consequences of Ras signaling are dependent upon cell-cycle position. In quiescent cells stimulated with growth factors, one Ras effector, phosphatidylinositol-3-kinase, is activated twice as cells transition from G(0) into G(1) phase, and then later in G(1) phase. It is only during the later stages of G(1) phase that PI3K activity promotes entry into S-phase. In cycling cells, Ras activity is enhanced throughout the cell cycle, but is able to stimulate cyclin D1 elevation only during G(2) phase.
authors.affiliation: Department of Molecular Biology, The Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA.
authors.forename: Dennis
authors.initials: D
authors.lastname: Stacey
authors.forename: Andrius
authors.initials: A
authors.lastname: Kazlauskas
mesh_terms: D000818:Animals; D002453:Cell Cycle / Q000502:physiology*; D019938:Cyclin D1 / Q000378:metabolism; D016193:G1 Phase; D005786:Gene Expression Regulation; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000502:physiology; D019908:Proto-Oncogene Proteins c-raf / Q000502:physiology; D016192:Resting Phase, Cell Cycle; D016196:S Phase; D015398:Signal Transduction / Q000502:physiology*; D020726:ral Guanine Nucleotide Exchange Factor / Q000502:physiology; D018631:ras Proteins / Q000378:metabolism / Q000502:physiology*
chemical_list: D020726:ral Guanine Nucleotide Exchange Factor; D019938:Cyclin D1; D019869:Phosphatidylinositol 3-Kinases; D019908:Proto-Oncogene Proteins c-raf; D018631:ras Proteins