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• W2096993973 abstract "Two distinct pathways for the degradation of mammalian cyclin E have previously been described. One pathway is induced by cyclin E phosphorylation and is dependent on the Cul1/Fbw7-based E3 ligase. The other pathway is dependent on the Cul3-based E3 ligase, but the mechanistic details of this pathway have yet to be elucidated. To establish the role of Cul3 in the degradation of cyclin E in vivo, we created a conditional knockout of the Cul3 gene in mice. Interestingly, the biallelic loss of Cul3 in primary fibroblasts derived from these mice results in increased cyclin E expression and reduced cell viability, paralleling the loss of Cul3 protein expression. Cell cycle analysis of viable, Cul3 hypomorphic cells shows that decreasing the levels of Cul3 increases both cyclin E protein levels and the number of cells in S phase. In order to examine the role of Cul3 in an in vivo setting, we determined the effect of deletion of the Cul3 gene in liver. This gene deletion resulted in a dramatic increase in cyclin E levels as well as an increase in cell size and ploidy. The results we report here show that the constitutive degradation pathway for cyclin E that is regulated by the Cul3-based E3 ligase is essential to maintain quiescence in mammalian cells." @default.
• W2096993973 created "2016-06-24" @default.
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• W2096993973 date "2007-05-01" @default.
• W2096993973 modified "2023-10-01" @default.
• W2096993973 title "Constitutive Turnover of Cyclin E by Cul3 Maintains Quiescence" @default.
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• W2096993973 doi "https://doi.org/10.1128/mcb.00720-06" @default.
• W2096993973 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1899986" @default.
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• W2096993973 hasPublicationYear "2007" @default.
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