7 results found
    1. Cell Biology
    2. Chromosomes and Gene Expression

    Fcp1 phosphatase controls Greatwall kinase to promote PP2A-B55 activation and mitotic progression

    Rosa Della Monica et al.
    The phosphatase Fcp1 inactivates Greatwall kinase at the end of mitosis.
    1. Cell Biology

    Homeostatic control of START through negative feedback between Cln3-Cdk1 and Rim15/Greatwall kinase in budding yeast

    Nicolas Talarek et al.
    Inhibition of phosphatases by kinases develops Whi5 phosphorylation and cell cycle function in low cyclin-dependent kinase activity.
    1. Computational and Systems Biology
    2. Neuroscience

    Reciprocal regulation of ARPP-16 by PKA and MAST3 kinases provides a cAMP-regulated switch in protein phosphatase 2A inhibition

    Veronica Musante et al.
    A complex interplay between MAST3 and PKA protein kinases and the regulatory protein ARPP-16 allows cAMP to control the activity of protein phosphatase 2A.
    1. Cell Biology

    Greatwall promotes cell transformation by hyperactivating AKT in human malignancies

    Jorge Vera et al.
    Greatwall is a new oncogene that induces AKT hyperphosphorylation by promoting the degradation of the phosphatase PHLPP.
    1. Biochemistry and Chemical Biology
    2. Cell Biology

    Unfair competition governs the interaction of pCPI-17 with myosin phosphatase (PP1-MYPT1)

    Joshua J Filter et al.
    Unfair competition, in which a phosphatase and a phosphoprotein inhibitor/substrate mutually sequester each other from competing substrates and enzymes, is a conserved mechanism for the control of PPP family phosphatases.
    1. Biochemistry and Chemical Biology
    2. Cell Biology

    Greatwall-phosphorylated Endosulfine is both an inhibitor and a substrate of PP2A-B55 heterotrimers

    Byron C Williams et al.
    The mechanism of inhibition by unfair competition is central to determining the protein phosphorylation states that govern cell cycle transitions between M phase and interphase.
    1. Cell Biology

    Spatiotemporal control of mitotic exit during anaphase by an aurora B-Cdk1 crosstalk

    Olga Afonso et al.
    Quantitative live-cell microscopy and molecular perturbations in Drosophila and human cells reveal a crosstalk between molecular 'rulers' (Aurora B) and 'clocks' (Cdk1) that coordinates mitotic exit in space and time.

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