William R. Foster

This study shows Greatwall kinase regulates AML cell division through a non-canonical pathway distinct from its role in solid tumors.

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.

This study shows that the balance between B55α and Greatwall expression levels determines cancer cell sensitivity to Greatwall inhibition.

The paper shows that the MIN motif in Rif2 inhibits MRN complex activity at telomeres, preventing DDR activation and NHEJ in yeast.