Abstract
The retinoblastoma protein, pRB, appears to play a key role in coordinating the regulation of cell cycle position and transcriptional events. pRB undergoes specific cell-cycle-dependent phosphorylation, being underphosphorylated in G1 and heavily phosphorylated in S, G2, and M. The underphosphorylated form is able to interact with the E2F transcription factor. Recently, we have cloned a cDNA for E2F-1. By using this clone and a series of non-pRB binding mutants, we have been able to show that the binding of pRB to E2F-1 causes inhibition of E2F-mediated transactivation. pRB's inhibition of E2F-mediated transcription would be lost by mutation in the retinoblastoma gene in human tumours, by pRB's interaction with DNA tumour virus oncoproteins, or by phosphorylation during the cell cycle.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenoviruses, Human / genetics
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Animals
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Carrier Proteins*
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Cell Cycle
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Cell Cycle Proteins*
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Chloramphenicol O-Acetyltransferase / biosynthesis
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Chloramphenicol O-Acetyltransferase / metabolism
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Cloning, Molecular
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DNA
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DNA-Binding Proteins*
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E2F Transcription Factors
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E2F1 Transcription Factor
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Phosphorylation
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Recombinant Fusion Proteins / biosynthesis
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Recombinant Fusion Proteins / metabolism
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Retinoblastoma Protein / biosynthesis*
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Retinoblastoma Protein / metabolism
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Retinoblastoma-Binding Protein 1
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Transcription Factor DP1
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Transcription Factors / biosynthesis
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Transcription Factors / metabolism*
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Transcription, Genetic*
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Transcriptional Activation
Substances
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Carrier Proteins
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Cell Cycle Proteins
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DNA-Binding Proteins
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E2F Transcription Factors
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E2F1 Transcription Factor
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Recombinant Fusion Proteins
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Retinoblastoma Protein
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Retinoblastoma-Binding Protein 1
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Transcription Factor DP1
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Transcription Factors
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DNA
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Chloramphenicol O-Acetyltransferase