Identification of a growth suppression domain within the retinoblastoma gene product.
- 1 June 1992
- journal article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 6 (6) , 953-964
- https://doi.org/10.1101/gad.6.6.953
Abstract
To date, all naturally occurring retinoblastoma susceptibility gene (RB) mutations known to be compatible with stable protein expression map to the T/E1A and cellular protein-binding region (the "pocket" domain). This domain extends from residue 379 to 792. When full-length RB and certain truncated forms were synthesized in human RB -/- cells, we found that the minimal region necessary for overt growth suppression extended from residue 379 to 928. A functional pocket domain and sequences extending from the carboxy-terminal boundary of the pocket to the carboxyl terminus of the protein were both necessary for growth suppression. Both sets of sequences were also required for E2F binding; hence, the two functions may be linked.Keywords
This publication has 44 references indexed in Scilit:
- The interaction of RB with E2F coincides with an inhibition of the transcriptional activity of E2F.Genes & Development, 1992
- Interaction of p107 with Cyclin A Independent of Complex Formation with Viral OncoproteinsScience, 1992
- G1/S phosphorylation of the retinoblastoma protein is associated with an altered affinity for the nuclear compartmentCell, 1991
- A cellular protein that competes with SV40 T antigen for binding to the retinoblastoma gene productNature, 1991
- Adenovirus E1A proteins can dissociate heteromeric complexes involving the E2F transcription factor: A novel mechanism for E1A trans-activationCell, 1990
- Suppression of Tumorigenicity of Human Prostate Carcinoma Cells by Replacing a Mutated RB GeneScience, 1990
- The retinoblastoma susceptibility gene product undergoes cell cycle-dependent dephosphorylation and binding to and release from SV40 large TCell, 1990
- The product of the retinoblastoma susceptibility gene has properties of a cell cycle regulatory elementCell, 1989
- Phosphorylation of the retinoblastoma gene product is modulated during the cell cycle and cellular differentiationCell, 1989
- Mutation and Cancer: Statistical Study of RetinoblastomaProceedings of the National Academy of Sciences, 1971