Journal
ONCOGENE
Volume 21, Issue 52, Pages 7923-7932Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1206001
Keywords
B-Myb; p107 pocket protein; cell cycle; cyclin E/Cdk2; cyclin A2/Cdk2
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B-Myb is a cell-cycle regulated transcription factor which is implicated in cell proliferation and has an essential role in early embryonic development. In this study we examined the functions of B-Myb required to overcome G1 arrest in Saos-2 cells induced by the retinoblastoma-related p107 protein. Our results demonstrated that this activity was independent of B-Myb transactivation function, but correlated with its capacity to form an in vivo complex with p107. A large proportion of B-Myb formed complexes with p107 in cotransfected cells, however, B-Myb bound weakly to the related p130 protein and not at all to pRb. In contrast to the E2F transcription factors, which bind the p107 C-terminal pocket domain, B-Myb recognizes an N-terminal p107 region which overlaps the larger cyclin-binding domain. B-Myb and cyclin A2 formed mutually exclusive complexes with p107, and B-Myb enhanced the activity of co-transfected cyclin E kinase activity, implying that B-Myb affects the cell cycle by preventing sequestration of active cyclin/cdk2 complexes. This study defines a novel function of B-Myb and further suggests that the p107 N-terminus provides an interaction domain for transcription factors involved in cell cycle control.
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