Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication

DOI

10.1038/352249a0

Type

Journal article

Journal

Nature

Publication Date

01/01/1991

Volume

352

Pages

249 - 251