[Control of cell proliferation by the retinoblastoma gene product].
Transformed cells proliferate abnormally, due to the unregulated activation of oncogenes and the inactivation of anti-oncogenes. The molecular mechanisms by which the product of the RB anti-oncogene, the RB protein, regulates cell proliferation begin to be understood. Major targets of RB include proteins involved in cell cycle entry, like the E2F transcription factor, and effectors of terminal differentiation. The effect of RB is thus to block cells into the G1 phase of the cell cycle and to induce them to terminally differentiate. Recently, a new role has been shown for RB. RB is able to repress the activity of the RNA polymerases I and III, thereby modulating the protein biosynthesis capacities of the cell. RB appears thus to control directly the balance between DNA and protein synthesis during the cell cycle.
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D002352:Carrier Proteins; D018797:Cell Cycle Proteins; D002455:Cell Division / Q000187:drug effects*; D004268:DNA-Binding Proteins; D050684:E2F Transcription Factors; D066298:In Vitro Techniques; D007399:Interphase / Q000187:drug effects; D016160:Retinoblastoma Protein / Q000494:pharmacology*; D056465:Retinoblastoma-Binding Protein 1; D013692:Telophase / Q000187:drug effects; D014157:Transcription Factors / Q000378:metabolism / Q000494:pharmacology
D002352:Carrier Proteins; D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D050684:E2F Transcription Factors; D016160:Retinoblastoma Protein; D056465:Retinoblastoma-Binding Protein 1; D014157:Transcription Factors
Contrôle de la prolifération cellulaire par le produit du gène de susceptibilité au rétinoblastome.