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.

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

A geneome-scale shRNA screen identifies five genes whose suppression promotes cell death upon PI3K inhibition both in vitro and in vivo, thus suggesting potential combination therapies involving PI3K inhibition.

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 unique two-step mechanism of plasma membrane recruitment and activation governs G-protein-coupled receptor mediated PI3K signaling.

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.

Ankyrin-B – through interactions with PI3P lipids, dynactin and RabGAP1L – functions as a critical node in the protein circuitry underlying polarized recycling of α5β1-integrin to enable haptotaxis along fibronectin gradients.

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

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