The brain-specific activator p35 allows Cdk5 to escape inhibition by p27Kip1 in neurons.
AUTOR(ES)
Lee, M H
RESUMO
Cell cycle withdrawal in postmitotic cells involves cyclin-dependent kinase (Cdk) inhibitors that repress cell cycle Cdk activity. During mouse neurogenesis, cortical postmitotic neurons are shown here to accumulate high levels of the p27 Cdk inhibitor compared with their progenitor neuroblasts. Elevated p27 levels in staged embryo brain extracts correlate with p27 binding to Cdk2, and Cdk inactivation. Yet, Cdk5, which is associated with the noncyclin activator p35 in neurons, remains active in the presence of high p27 levels. Both in vitro and in vivo, p27 and related inhibitors can recognize a cyclin D-Cdk5 complex but not a p35-Cdk5 complex. The results indicate that the choice of activator determines the susceptibility of Cdk5 to p27 and related Cdk inhibitors, and thus its ability to act in postmitotic cells.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=39593Documentos Relacionados
- Cdk5 Regulates the Organization of Nestin and Its Association with p35
- Cooperation between the Cdk inhibitors p27KIP1 and p57KIP2 in the control of tissue growth and development
- Density-dependent Growth Inhibition of Fibroblasts Ectopically Expressing p27kip1
- Gene disruption of p27Kip1 allows cell proliferation in the postnatal and adult organ of Corti
- Targeted Disruption of CDK4 Delays Cell Cycle Entry with Enhanced p27Kip1 Activity