The protein kinase HIPK2 is activated by DNA damage signalling and controls cell fate by activating cell death-stimulating gene expression upon exposure to severe DNA damage. Our unpublished work has identified an unforeseen role of HIPK2 upon mild, repairable DNA damage, where it localises to DNA double-strand breaks and appears to act on a different set of substrates. In this project, we therefore aim at dissecting the mechanisms of pathway choice between DNA repair versus cell death in response to DNA damage. By combining genomic, proteomic and molecular approaches, we expect to elucidate the function of HIPK2 in this decision.
Dissecting the mechanism underlying repair versus cell death pathway choice upon DNA damage