Calin-Mihai Dragoi

The paper investigates how perturbations of the CDK1-Greatwall-PP2A-B55 feedback loop affect cell-cycle control in different cell types, finding that PP2A-B55 acts as a context-dependent G2/M repressor and that cancer cells show specific sensitivities to PKMYT1 inhibitors.

The paper models the eukaryotic cell cycle as a tetra-stable excitable system using ODEs, phase plane analysis, and bifurcation theory, showing that two existing frameworks represent the same underlying architecture.

This study identifies a new role for Wee1 in promoting S-phase entry by inhibiting APC/CCdh1, revealing a mechanism that impacts the efficacy and toxicity of Wee1 inhibitors in cancer treatment.

The paper develops a dynamical model of the cell cycle as two mutually inhibitory oscillators, showing how this framework can explain various cell cycle behaviors.

This paper shows that dysregulation of CycB:CDK disrupts cell cycle switches, leading to genome doubling, a common event in tumorigenesis.