title: From growth to cell cycle control.
abstract: How does a quiescent cell decide to re-enter the cell cycle and start replicating its DNA? What controls cell proliferation? These are fundamental questions that have to be solved in order to understand the mechanisms of oncogenesis. Some recent data have provided clues about how signal transduction pathways may be connected to the cell cycle. A protein kinase cascade starting from the membrane growth factor receptor is thought to be involved in transducing extracellular stimuli to the master switches of the cell cycle control machinery. The recently identified extracellular-signal regulated kinases (ERKs) appear to play an important role in this pathway. Expression of cyclins, which are regulatory subunits of the universal cell cycle oscillator cdc2, may also be controlled through this kinase cascade. The products of tumor suppressor genes Rb and p53 also play an important role in regulating cell proliferation by interfering with the cell cycle pathway. Here, I will review and discuss the importance of these different new results.
authors.affiliation: E.M.B.L. Differentiation Programme, Heidelberg, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Ducommun
mesh_terms: D000818:Animals; D016203:CDC2 Protein Kinase / Q000378:metabolism; D002453:Cell Cycle / Q000502:physiology*; D016213:Cyclins / Q000502:physiology; D004261:DNA Replication / Q000502:physiology; D006801:Humans; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D010766:Phosphorylation; D016160:Retinoblastoma Protein / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D016213:Cyclins; D008869:Microtubule-Associated Proteins; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D016203:CDC2 Protein Kinase