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Research programme 02

DNA-damage checkpoints

We define how p53 coordinates reversible arrest, mitotic entry and recovery after transient or sustained genotoxic stress.

The laboratory has long investigated p53-dependent control of G1 and G2/M checkpoints. This work connects transcriptional repression of mitotic regulators with post-transcriptional mechanisms that determine whether damaged cells arrest, repair or die.

Representative targets include CDC25C, survivin, CDC20 and cyclin B1. Their regulation provides a mechanistic route to understand why p53-defective tumor cells respond differently to DNA-damaging treatment.

dm2 contributes to cell cycle arrest and prevents apoptosis.Following stress, p53 activates different transcriptional programs resultingin cell cycle arrest or apoptosis.
dm2 contributes to cell cycle arrest and prevents apoptosis.Following stress, p53 activates different transcriptional programs resultingin cell cycle arrest or apoptosis.
Next programme Cell-fate decisions