A. T. Saurin

Oncogenic signals prime cancer cells for toxic cell growth during a G1 cell cycle arrest

This paper shows CDK4/6 inhibitors cause toxic cell growth in cancer cells during G1 arrest due to oncogenic signals, which can be reversed by targeting mTOR.

The search for CDK4/6 inhibitor biomarkers has been hampered by inappropriate proliferation assays

This paper shows that ATP-based proliferation assays overestimate CDK4/6 inhibitor response due to G1 cell overgrowth, and identifies Cyclin D1 and RB1 as potential biomarkers using DNA-based assays.

Cell overgrowth during G1 arrest triggers an osmotic stress response and chronic p38 activation to promote cell cycle exit

The paper shows that CDK4/6 inhibitor-induced G1 arrest causes cell overgrowth, triggering osmotic stress and p38-p53-p21 signaling to promote cell cycle exit.

A bifunctional kinase-phosphatase module integrates mitotic checkpoint and error-correction signalling to ensure mitotic fidelity

This study shows that the PLK1-PP2A kinase-phosphatase pair regulates mitotic checkpoint and error-correction signaling through feedback on the BUB complex, ensuring proper chromosome segregation.

CDK4/6 inhibitors induce replication stress to cause long-term cell cycle withdrawal

This study shows CDK4/6 inhibitors cause long-term cell cycle withdrawal by inducing replication stress and p53-dependent effects, linking them to genotoxic stress and potential combination therapies.

A spatio-temporal mathematical model for the dynamics of paclitaxel in cell monolayers.

The paper presents a spatio-temporal mathematical model for paclitaxel dynamics in cell monolayers but retracts due to fundamental issues in the ODE/PDE implementation.

Kinetochore phosphatases suppress autonomous kinase activity to control the spindle assembly checkpoint

The paper shows that kinetochore phosphatases suppress PLK1 activity to dephosphorylate MELT motifs on KNL1, thereby removing SAC proteins like the BUB complex from kinetochores.

Cyclin B1 scaffolds MAD1 at the corona to activate the spindle assembly checkpoint

This study identifies Cyclin B1 as a scaffold that localizes MAD1 to the kinetochore corona, enabling the spindle assembly checkpoint by making MAD1 phosphorylation independent of MPS1.

PP1 and PP2A use opposite phospho-dependencies to control distinct processes at the kinetochore

The paper shows PP1 and PP2A-B56 use opposite phospho-dependencies to control distinct mitotic processes at the kinetochore through differential kinase input responses.

Division of labour between different PP2A-B56 complexes during mitosis

This study identifies how different PP2A-B56 isoforms localise to distinct mitotic structures through specific protein interactions, controlling key mitotic processes.