University, Tel Aviv | Israel
EMBO 2002 | FelC 06–09
We are interested in the mechanisms that maintain genome stability and the link between genome stability, human diseases and aging. Our work is focused on the ATM-mediated signaling network, which is activated by DNA damage. ATM is a powerful protein kinase that is absent in patients with the genome instability syndrome, ataxia-telangiectasia (A-T). We are also interested in the molecular pathology of the cerebellar degeneration in A-T.
Keywords: DNA damage response / genome stability / ATM / ataxia-telangiectasia / neurodegeneration / genetic predisposition to cancer / aging