The G2 DNA damage checkpoint

Funded Activity Summary

Normal healthy cells reproduce themselves with a remarkable fidelity. This ensures the stable inheritance of our genetic material, or DNA, and is essential for normal tissue development and maintenance. Cancer cells, on the contrary, show a high degree of rearrangements to their chromosomes, the bodies that hold the DNA. This is a result of a process known as genomic instability. This instability allows normal cells to become cancerous through the accumulation of a number of genetic changes. This project looks at a biochemical pathway, called the G2 DNA damage checkpoint, which functions in cells to prevent cell division when the chromosomes have been damaged. Once they have been repaired, this brake is relieved, and the cells will then divide without genetic alterations. We are concentrating our studies on an enzyme, called chk1, which is the final point of this pathway. Chk1 biochemically modifies the proteins that control cell division, and stops them from carrying out their normal function when the chromosomes are damaged. Our work will determine how chk1 is told by the cell to carry out this function, and how failure to do so leads to cancer.

Funded Activity Details

Start Date: 01-01-2001

End Date: 01-01-2003

Funding Scheme: NHMRC Project Grants

Funding Amount: $408,055.00

Funder: National Health and Medical Research Council

Research Topics

ANZSRC Field of Research (FoR)

Cell Development (Incl. Cell Division And Apoptosis)

ANZSRC Socio-Economic Objective (SEO)

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Other Keywords

Cancer Detection, therapy and prevention | Cell Cycle Control | G2 DNA damage checkpoint | Genetic Abnormalities | Genomic Instability | Radiation Biology | Signal Transduction | Yeast Genetics

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