Investigation of the interplay between SKP2, CDT1 and Geminin in cancer cells
- Published
- Accepted
- Subject Areas
- Biochemistry, Cell Biology, Molecular Biology
- Keywords
- SKP2, CDT1, Geminin, DNA replication, Cell cycle, CDK, CDC7
- Copyright
- © 2015 Ballabeni et al.
- Licence
- This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ PrePrints) and either DOI or URL of the article must be cited.
- Cite this article
- 2015. Investigation of the interplay between SKP2, CDT1 and Geminin in cancer cells. PeerJ PrePrints 3:e794v1 https://doi.org/10.7287/peerj.preprints.794v1
Abstract
Geminin has a dual role in the regulation of DNA replication: it inhibits replication factor CDT1 activity during the G2 phase of the cell cycle and promotes its accumulation at the G2/M transition. In this way Geminin prevents DNA re-replication during G2 phase and ensures that DNA replication is efficiently executed in the next S phase. CDT1 was shown to associate with SKP2, the substrate recognition factor of the SCF ubiquitin ligase complex. We investigated the interplay between these three proteins in cancer cell lines. We show that Geminin, CDT1 and SKP2 could possibly form a complex and propose the putative regions of CDT1 and Geminin involved in the binding. We also show that, despite the physical interaction, SKP2 depletion does not substantially affect CDT1 and Geminin protein levels. Moreover, we show that while Geminin and CDT1 levels fluctuate, SKP2 levels, differently than in normal cells, are almost steady during the cell cycle of the tested cancer cells.
Author Comment
We submit this research article entitled “Investigation of the interplay between SKP2, CDT1 and Geminin in cancer cells” to PeerJ PrePrints. We believe that the data contained in this paper provide valuable new information about the relationship between these cell cycle regulators. Though additional data will be needed to fully confirm the models proposed in the paper, in the spirit of open science and open collaboration we would like to submit the existing data as we believe they could be useful to the scientists working on these three proteins.