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lüll Pathways governing G1/S transition and their response to DNA damage Bartek J; Lukas JFEBS Lett 2001[Feb]; 490 (3): 117-22The ability to self-replicate is a fundamental feature of life, reflected at the cellular level by a highly regulated process initiated in G1 phase via commitment to a round of DNA replication and cell division. Here we briefly highlight recent advances in understanding the molecular pathways which govern the decision of mammalian somatic cells to enter S phase, and the so-called cell cycle checkpoints which guard the G1/S transition and S phase progression against potentially deleterious effects of genotoxic stress. Particular emphasis is put on the emerging parallel yet cooperative pathways of retinoblastoma protein (pRB)-E2F and Myc, their convergence to control the activity of the cyclin-dependent kinase 2 (Cdk2) at the G1/S boundary, as well as the two waves of checkpoint responses at G1/S: the rapid pathway(s) leading to Cdc25A degradation, and the delayed p53-p21 cascade, both silencing the Cdk2 activity upon DNA damage.|*CDC2-CDC28 Kinases[MESH]|*Carrier Proteins[MESH]|*Cell Cycle Proteins[MESH]|*DNA-Binding Proteins[MESH]|*G1 Phase[MESH]|*S Phase[MESH]|Animals[MESH]|Cell Division[MESH]|Cyclin E/metabolism[MESH]|Cyclin-Dependent Kinase 2[MESH]|Cyclin-Dependent Kinase Inhibitor p21[MESH]|Cyclin-Dependent Kinases/metabolism[MESH]|Cyclins/metabolism[MESH]|DNA Damage/*genetics[MESH]|E2F Transcription Factors[MESH]|Neoplasms/genetics/pathology[MESH]|Protein Serine-Threonine Kinases/metabolism[MESH]|Proto-Oncogene Proteins c-myc/metabolism[MESH]|Retinoblastoma Protein/metabolism[MESH]|Retinoblastoma-Binding Protein 1[MESH]|Signal Transduction[MESH]|Transcription Factors/metabolism[MESH]|Tumor Suppressor Protein p53/metabolism[MESH] |