ST recruitment of STRIPAK facilitates PP2A-mediated dephosphorylation of MAP4K4 and induces cell transformation highlighting that STRIPAK complex plays a key role in defining PP2A specificity and activity.

Tgfb3 inhibits Muller glial cell reprogramming and drives Muller cell quiescence in the injured zebrafish retina, thereby inhibiting retina regeneration.

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

Distinct PP2A-B56 complexes use isoform-selective interactions to localise to either the centromere or kinetochore and control different processes during mitosis.

The scaffold protein SAV1 counteracts PP2A to activate Hippo kinases.

A comprehensive whole cell proteomic map describing expression time courses of >6,500 viral and cellular proteins during HIV infection identifies Vif-dependent antagonism of key cellular phosphatase PP2A.

A novel dynamic charge-charge interaction between B56 and a subset of PP2A-B56 substrates is essential for substrate specificity, dephosphorylation and, for KIF4A, binding condensin I.

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.

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.