Abstract
Cyclin A-kinase, an enzyme required for coordinating S phase progression, forms stable in vivo complexes with E2F-1, a growth-promoting transcription factor, which binds to the retinoblastoma gene product and is involved in the timely activation of genes whose products contribute to G1 exit and S phase traversal. Complex formation results in a negative biochemical effect of cyclin A-kinase: the shut-off of E2F-1-dependent DNA binding function in S/G2. Thus, specific and timely cell cycle-dependent interactions of E2F-1 with proteins that inhibit its function (i.e., RB during G1 and cyclin A-kinase during S/G2) may contribute to the periodicity of expression of certain E2F-1-responsive genes at the G1/S transition.
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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3T3 Cells
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Amino Acid Sequence
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Animals
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Carrier Proteins*
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Cell Cycle / physiology*
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Cell Cycle Proteins*
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Cell Line
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Cyclins / genetics
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Cyclins / metabolism*
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DNA / metabolism
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism
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E2F Transcription Factors
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E2F1 Transcription Factor
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Gene Expression Regulation
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Humans
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Mice
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Molecular Sequence Data
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Precipitin Tests
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Protein Binding
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Protein Kinases / metabolism*
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Protein Structure, Tertiary
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Recombinant Fusion Proteins / metabolism
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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 / genetics
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Transcription Factors / metabolism*
Substances
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Arid4a protein, mouse
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Carrier Proteins
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Cell Cycle Proteins
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Cyclins
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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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E2F1 protein, human
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E2f1 protein, mouse
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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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Protein Kinases