The c-terminus of PI3K plays a key role in regulating kinase activity, with c-terminal disease-linked mutations leading to either activation or inhibition, which reveal a path to specific inhibitors.

Two of the most commonly mutated growth factor pathways induce a deadly feature of lung adenocarcinoma.

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

Sterol transport by Niemann-Pick type C proteins induces the expansion of raft-like domains in the yeast vacuole, enabling engulfment of lipid droplets by microautophagy.

A signalling cascade involving PI3K/Akt1 remodels the extra-cellular matrix to achieve atypical cellular responses and control cell fate specification within the embryonic endoderm.

Embryonic PI3K-Yap activity regulates apical adhesion and proliferation of neural progenitors lining the lateral ventricular surface, to maintain the smooth, non-folded mouse brain and to prevent developmental hydrocephalus.

Variation in the rate of mixed infections by malaria parasites and the relatedness structure among infecting strains reveals diversity in local epidemiological processes.

The malaria parasite Niemann-Pick Type C1-related protein is an important new antimalarial target.

High PI3K-Akt-mTORC1 activity inhibits Schwann cell differentiation, while after onset of myelination, residual PI3K-Akt-mTORC1 activity promotes myelin growth.

Antagonistic signaling by the kinases PI3K and Itpkb limits the kinetics and enforces the Notch-dependence of beta-selection – the most important cell-fate determining process in alpha beta T cell development.