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THE retinoblastoma gene (Rb) product is a negative regulator of cellular proliferation1, an effect that could be mediated in part at the transcriptional level through its ability to complex with the sequence-specific transcription factor DRTF1 (ref. 2). This interaction is modulated by adenovirus El a, which sequesters the Rb protein3 and several other cellular proteins<3>, including cyclin A (refs 4, 5), a molecule that undergoes cyclical accumulation and destruction during each cell cycle6, 7 and which is required for cell cycle progression8. Cyclin A, which also complexes with DRTF1, facilitates the efficient assembly of the Rb protein into the complex. This suggests a role for cyclin A in regulating transcription and defines a transcription factor through which molecules that regulate the cell cycle in a negative fashion, such as Rb, and in a positive fashion, such as cyclin A, interact. Mutant loss-of-function Rb alleles, which occur in a variety of tumour cells, also fail to complex with Ela and large T antigen9, 10. Here we report on a naturally occurring loss-of-function Rb allele encoding a protein that fails to complex with DRTF1. This might explain how mutation in the Rb gene prevents negative growth control. © 1991 Nature Publishing Group.

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Journal article



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249 - 251