Kathy Friedman lab
Double Strand Breaks (DSBs) are a common threat to Eukaryotic genome stability and cell viability. Two of the primary mechanisms by which the cell repairs DSBs are Homologous Recombination (HR) and Non-homologous End Joining (NHEJ). The protein Rif1, initially identified as a telomere binding protein in yeast, has been recently implicated in NHEJ; however its role remains incompletely understood. The focus of my research is to uncover the role(s) of Rif1 in NHEJ, and the mechanism of its action.