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Journal Club
The Cyclin D3 Knockout: A Pound of Redundancy with a Dash of Tissue Specificity
J. Alan Diehl
volume 3 | issue 2
feb 2004Pages: 162-164
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Progression through each phase of the cell division cycle is driven by specific cyclin/CDK holoenzymes complexes, each complex having a discrete subset of critical substrates. Phosphorylation of these substrates by the appropriate cyclin/CDK complex in turn directs regulated cell cycle progression. Based on this notion, a reasonable assumption is that elimination of any one of these complexes would be catastrophic with regard to cellular and organismal development. Over the past year however, we have witnessed elegant work that challenges the notion that cyclin/CDK holoenzymes target unique and specific substrates. Indeed in the most recent work, Sicinska et al. report that targeted deletion of the G1 cyclin, cyclin D3, disrupts proliferation of immature T lymphocytes, but does not provide a function essential for organismal development or survival.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDFIf the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.