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- W1008077541 abstract "The faithful transmission of the genetic material to the daughter cells requires extreme accuracy in DNA replication, precision in chromosome distribution and effective repair mechanisms to minimize heritable mutations affecting the genetic material. To achieve this fidelity, cells have evolved surveillance mechanisms that monitor the structure of DNA and coordinate repair and cell cycle progression. Recent studies revealed that Cdt1 is a critical and evolutionarily conserved target of the DNA damage checkpoint, since exposure to ionizing or UV radiation targets Cdt1 for degradation. Cdt1 is an essential component of the cell cycle licensing machinery that is conserved from yeasts to mammals.We have examined the ability of several anticancer drugs to act through the Cdt1 dependent cell cycle checkpoint. Our findings indicate that DNA damage induced by MMS, Cisplatin and Doxorubicin leads to rapid proteolytic destruction of Cdt1, whereas treatment with Tamoxifen does not affect Cdt1 protein levels. DNA damage induced by Etoposide has differential effect on Cdt1 protein levels, depending on the cell line. There is no change on Geminin expression levels, the protein inhibitor of Cdt1. Our results suggest that genotoxic therapies used against cancer differ in respect to Cdt1 dependent checkpoint." @default.
- W1008077541 created "2016-06-24" @default.
- W1008077541 creator A5004872851 @default.
- W1008077541 date "2008-04-04" @default.
- W1008077541 modified "2023-09-24" @default.
- W1008077541 title "Μελέτη της επίδρασης αντικαρκινικών χημειοθεραπευτικών φαρμάκων στη ρύθμιση του Cdt1" @default.
- W1008077541 hasPublicationYear "2008" @default.
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