A protein kinase complex that is important for cell division is lost in testicular seminoma, which is a common cancer in men.

Maternal embryonic leucine zipper kinase (MELK) is a new anti-cancer target that is highly selective for basal-like breast cancer.

Replication stress-indepedent synthetic lethality can be triggered in BRCA2-deficient cells by exploiting M phase defects.

The phosphatase Fcp1 inactivates Greatwall kinase at the end of mitosis.

By distributing regulation to both the GTPase and downstream kinases, the Mitotic Exit Network creates a single signal from spatial and temporal inputs.

Phosphorylation of Aurora A does not trigger a population shift to the active state as previously thought, but instead switches the kinase on by tuning the structure and dynamics of a dynamically sampled subpopulation.

Building on previous work (Booth et al, 2014), we show how two mitotic phosphatases are formed, how they are regulated by opposing kinases during the cell cycle and reveal a novel opportunity for the development of cancer therapeutics.

The human NimA-related kinases (Neks) recognize divergent substrate motifs, and include Nek10 as a dual-specificity serine/tyrosine kinase, and Nek6, Nek7 and Nek9 as amplifiers of the Plk1 phospho-motif.

Genetically-encoded platforms direct kinase inhibitor drugs to organelles to reveal new dimensions of local kinase signaling.

The microtubule organizing potential of the centrosome is inactivated in a stepwise process through phosphatase activity and mechanical disruption to remove an aging matrix of proteins.