Loss of Cul1 results in early embryonic lethality and dysregulation of cyclin E
Copyright policy )Loss of Cul1 results in early embryonic lethality and dysregulation of cyclin E
The sequential timing of cell-cycle transitions is primarily governed by the availability and activity of key cell-cycle proteins. Recent studies in yeast have identified a class of ubiquitin ligases (E3 enzymes) called SCF complexes, which regulate the abundance of proteins that promote and inhibit cell-cycle progression at the G1-S phase transition. SCF complexes consist of three invariable components, Skp1, Cul-1 (Cdc53 in yeast) and Rbx1, and a variable F-box protein that recruits a specific cellular protein to the ubquitin pathway for degradation. To study the role of Cul-1 in mammalian development and cell-cycle regulation, we generated mice deficient for Cul1 and analysed null embryos and heterozygous cell lines. We show that Cul1 is required for early mouse development and that Cul1 mutants fail to regulate the abundance of the G1 cyclin, cyclin E (encoded by Ccne), during embryogenesis.
- University of California, San Francisco United States
- University of California, San Diego United States
- University of Georgia Press United States
- University of Georgia Georgia
- University of California System United States
Male, Cell Death, Molecular Sequence Data, Gene Expression Regulation, Developmental, Cell Cycle Proteins, Cullin Proteins, Embryo, Mammalian, Immunohistochemistry, Embryonic and Fetal Development, Mice, Cyclin E, Mutation, In Situ Nick-End Labeling, Animals, Humans, Female, Fetal Death, Cell Division, Cells, Cultured, In Situ Hybridization
Male, Cell Death, Molecular Sequence Data, Gene Expression Regulation, Developmental, Cell Cycle Proteins, Cullin Proteins, Embryo, Mammalian, Immunohistochemistry, Embryonic and Fetal Development, Mice, Cyclin E, Mutation, In Situ Nick-End Labeling, Animals, Humans, Female, Fetal Death, Cell Division, Cells, Cultured, In Situ Hybridization
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