University, Tel Aviv | Israel
EMBO 2002 | FelC 06–09
We are interested in the mechanisms that maintain genomic stability. 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 genomic instability syndrome, ataxia-telangiectasia (A-T). Another focus of interest in the lab is the molecular pathology of neurodegeneration in A-T.
Keywords: DNA damage response / genome stability / ATM / ataxia-telangiectasia / cell cycle checkpoints / genetic predisposition to cancer / aging