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.

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.

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.

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

Fetus and trophoblast interplay to regulate fetal nutrient supply and, ultimately, affect healthy growth.

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.