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Cancer Lett. 2001 Sep 28;171(1):87-101.

B-myb rescues ras-induced premature senescence, which requires its transactivation domain.

Author information

1
Division of Molecular Carcinogenesis and Center for Biomedical Genetics, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, The Netherlands.

Abstract

B-myb, a ubiquitously expressed member of the myb gene family, is highly regulated throughout the cell cycle and appears to be required for cell cycle progression. In contrast to its relatives A-myb, c-myb, and v-myb, no transforming activity of B-myb has been reported thus far. We report here that B-myb can rescue senescence induced by an activated ras oncogene in rodent cells in vitro. We show that transformation by B-Myb involves its ability to activate transcription. Similar to other oncogenic transcription factors, such as c-Myc and E2F, we show that B-Myb also has repression activity. We demonstrate that the C-terminus of B-Myb can function as a repressor of transcription, that B-Myb interacts with the repressor molecules BS69 and N-CoR and that the repression function, like the transactivation domain, contributes to B-myb transformation.

PMID:
11485831
[Indexed for MEDLINE]

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