Research programme 03

Cell-fate decisions

We study how p53-dependent gene regulation is integrated with p21, apoptotic pathways and cellular cofactors to choose arrest, senescence or death.

A therapeutically useful p53 response depends not only on whether the pathway is activated, but on the cellular outcome that follows. The laboratory investigates how p21, basal apoptotic regulators and transcriptional cofactors shift this balance.

This programme links promoter architecture, cofactor usage and stress context to the final phenotype, with the goal of understanding resistance to genotoxic cancer therapy.

Cellular stress induces p53‐dependent responses. In response to cellular stress such as DNA damage, the p53 protein becomes stabilized. In the nucleus, p53 binds to specific promoters and activates transcription of its target genes.

Next programme The p53 regulatory network →