PTEN organizes multicellular architecture by non-catalytic scaffolding of spatially localized β-Arrestin1/ARHGAP21/Cdc42 protein complexes to control mitotic spindle orientation, multicellular configuration and lumen formation.

A theory is presented for the optimal design of cellular sensing systems that maximizes the sensing precision given resource constraints.

PTEN mutations disrupt inhibitory GABAergic signaling, causing neurodevelopmental defects that can be mitigated by β-hydroxybutyrate, which activates DAF-16/FOXO and may offer a therapeutic approach for excitation/inhibition imbalances.

The p85α homodimer plays a role in the PI3K pathway by regulating PTEN function.

C-terminal phosphorylation of the lipid phosphatase PTEN drives a reduction in membrane affinity and leads to a more compact conformation that involves a C2 domain-tail interaction.

Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.

Signals conveyed from two different senses from a given point in space converge onto the same neurons of the optic tectum that trigger the gaze-control-system, and at the same time inhibit other parts of the tectal motor map.

An oscillating computational model combined with a predictive internal linguistic model can track naturally timed speech in which pseudo-rhythmicity is related to the predictability of words within their sentence context.

DNA-PK and PTEN protect breast cancer cells from lethal replication stress induced by the WEE1 inhibitor AZD1775 and constitute new potential biomarkers for AZD1775 sensitivity.