Phosphorylation and activation of B-Myb by cyclin A-Cdk2.
Curr Biol
; 7(4): 253-60, 1997 Apr 01.
Article
em En
| MEDLINE
| ID: mdl-9094315
ABSTRACT
BACKGROUND:
Cyclins and their catalytic partners, the cyclin-dependent kinases (Cdks), function as key regulators of the eukaryotic cell cycle. Specific cyclin-Cdk complexes are active at successive stages during the cell cycle and control cell-cycle progression by phosphorylating specific target proteins, most of which have not yet been identified. B-Myb, a conserved member of the Myb oncoprotein family, is a sequence-specific DNA-binding protein expressed in virtually all proliferating mammalian cells. Increasing evidence suggests that B-Myb plays an important role during the late G1 and early S phases of the cell cycle. In this study, we have examined the regulation of B-Myb activity by cyclin-Cdks.RESULTS:
We found that the transcriptional transactivation potential of B-Myb was repressed by a regulatory domain located at the carboxyl terminus of the protein. Coexpression of B-Myb and cyclin A relieved this repression by phosphorylation of B-Myb in its carboxy-terminal region. Tryptic phosphopeptide mapping revealed that endogenous B-Myb was phosphorylated in cells undergoing S phase.CONCLUSIONS:
This work provides evidence for a link between the Myb oncoprotein family and the cell-cycle machinery. We have shown that the carboxyl terminus of B-Myb acts as a cell-cycle sensor that regulates the transactivation function of B-Myb. Moreover, our studies have identified B-Myb as a target of cyclin A-Cdk2 and have indicated that B-Myb activity is regulated by phosphorylation mediated by cyclin A-Cdk2.
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Base de dados:
MEDLINE
Assunto principal:
Fatores de Transcrição
/
Ciclo Celular
/
Transativadores
/
Proteínas Serina-Treonina Quinases
/
Ciclinas
/
Quinases Ciclina-Dependentes
/
Proteínas de Ciclo Celular
/
Proteínas de Saccharomyces cerevisiae
/
Quinases relacionadas a CDC2 e CDC28
/
Proteínas de Ligação a DNA
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
1997
Tipo de documento:
Article