Cell cycle promoting activity of JunB through cyclin A activation - PubMed (original) (raw)
. 2002 Sep 27;277(39):35961-8.
doi: 10.1074/jbc.M202847200. Epub 2002 Jul 16.
Affiliations
- PMID: 12121977
- DOI: 10.1074/jbc.M202847200
Free article
Cell cycle promoting activity of JunB through cyclin A activation
Sven Andrecht et al. J Biol Chem. 2002.
Free article
Abstract
JunB, a major component of the AP-1 transcription factor, is known to act antagonistically to c-Jun in transcriptional regulation and is proposed to be a negative regulator of cell proliferation. Employing fibroblasts derived from E9.5 junB(-/-) mouse embryos we provide evidence for a novel cell cycle promoting role of JunB. Despite a normal proliferation rate, primary and immortalized junB(-/-) fibroblasts exhibited an altered cell cycle profile, which was characterized by an increase in the population of S-phase cells, while that of cells in G(2)/M-phase was diminished. This delay in G(2)/M-transition is caused by impaired cyclin A-CDK2 and cyclin B-CDC2 kinase activities and counteracts the accelerated S-phase entry. Cells lacking JunB show severely delayed kinetics of cyclin A mRNA expression due to the loss of proper transcriptional activation mediated via binding of JunB to the CRE element in the cyclin A promoter. Upon reintroduction of an inducible JunB-ER(TM) expression vector the cell cycle distribution and the cell cycle-associated cyclin A-CDK2 kinase activity could be restored. Thus, cyclin A is a direct transcriptional target of JunB driving cell proliferation.
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