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During the S/G2 phase of the cell cycle DNA double-strand breaks (DSBs) are preferentially repaired by homologous recombination (HR), a process that depends on the search and invasion into a homologous template sequence. These steps are carried out by the recombinase RAD51 and are facilitated by various RAD51-interacting proteins. In my research I explore synthetic lethalities between RAD51-interacting proteins, and their implications for homologous recombination deficiency.