The DNA damage response pathway is essential for the maintenance of genomic stability. Dysfunctional DNA damage response is linked to genomic instability, a driving force for carcinogenesis. When a cell faces DNA damage (e.g. provoked by irradiation, reactive oxygen species, shortened telomeres, chemotherapeutic drugs), a network of evolutionary conserved signaling pathways is activated which coordinate the cellular response to DNA damage. Dependent on the cell type and the degree of damage, this results in the activation of divergent cellular effector pathways leading to cell cycle checkpoint activation, DNA repair, apoptosis and cellular senescence. How the cellular decision-making between the divergent effector pathways is regulated is currently incompletely understood.

To gain insight in the DNA damage effector pathway decision, our goal is to identify novel components of DNA damage signaling and to characterize their role in the DNA damage response.