|Year of selection||2010|
|Institution||University of Kyoto|
Type of support
60 000 €
Back to basics: a trip down cancer pathways
When discussing cancer, balance is everything. p53, a gene famous for its mood swings, can either start or stop tumors. Whether pre-cancerous cells lean towards survival or death depends a lot on what p53 proteins do and how much they do it. Interestingly, Dr. Candeias has revealed that levels of p53 proteins are regulated by… p53 itself! Or, rather, by p53 messenger RNA (mRNA), the intermediary which gives instructions to make p53 proteins. Unorthodoxly, the molecule happens to protect from destruction the very proteins that it makes. A kick in the guts of molecular biology doctrines that explains some of p53’s fancies: even with operational proteins, malfunctioning RNA could deregulate the cell’s fragile equilibrium. Grasp of the nuts and bolts of mRNA multi-functionality could open way for cancer treatments that target only the desired functions of p53 and avoid secondary side effects.
My research focuses on the protein p53, a key mediator of the DNA damage response which controls genome stability and cancer development. My aim is to verify the importance of the p53 mRNA (messenger RNA) – Mdm2 interaction in controlling the protein Mdm2 and p53 functions. This study holds promise to offer a viable explanation to why induction of Mdm2 by p53 in response to DNA damage leads to an actual increase in p53 activity and not to p53 inactivation.
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