The retinoblastoma family member p107 binds to B-MYB and suppresses its autoregulatory activity.
It was recently reported that B-MYB can overcome p107-induced growth arrest. Here we show that B-MYB autoregulation of its own transcription is specifically suppressed by p107 and transient transfection assays with p107 deletion constructs determined that the carboxyl terminus of the protein, containing the major pocket region, was associated with inhibition of B-MYB-dependent transactivation. Consistent with these results, co-immunoprecipitation studies showed that p107 interacted in vivo with B-MYB through its pocket and carboxyl terminus domain. Thus, B-MYB-dependent promotion of cell proliferation and gene transactivation might be specifically repressed by the growth suppressor p107 through direct interaction with B-MYB.
Kimmel Cancer Institute, Department of Microbiology-Immunology, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA.
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Sala
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De Luca
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Giordano
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Peschle
D018797:Cell Cycle Proteins; D002455:Cell Division; D002460:Cell Line; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D011485:Protein Binding; D015534:Trans-Activators; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*; D015533:Transcriptional Activation
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D015534:Trans-Activators; D014157:Transcription Factors