When challenged by energetic stresses triggered by hypoxia and ATP inhibition, plasma membrane PI4P and PIP2 in cells undergo dramatic turnovers that have profound impact on many cellular processes including electrostatic PM targeting of numerous polybasic proteins.

TRPV4 channels in brain capillaries are suppressed by the phosphoinositide PIP2 and activated by receptor agonists implicated in neurovascular coupling.

The autophagosomal membrane becomes negatively charged during maturation due to the accumulation of PI4P, leading to the recruitment of syntaxin 17, which is required for autophagosome-lysosome fusion.

A Notch-mediated signaling pathway upregulates a Sec14-GOLD phosphopholipid binding protein that promotes a morphogenetic process important in tissue remodeling and renewal.

This work validates PIP4K gamma as pharmacological target to ameliorate Huntington's disease.

P-Rex1 adopts an inactive, compact conformation that is stabilized by an abundant intracellular molecule and undergoes dynamic changes to extend upon encountering signaling phospholipids in membranes.

Unprecedented resolution of the molecular mechanisms of plant membrane protein anchoring involving phospholipids and sterols reveals the control of spatio-temporal segregation into plasma membrane nanodomains.

The PRMT1 protein mediates arginine methylation of KCNQ2 channels to control neuronal excitability.

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.

The anchoring properties of Ca_V β2 subunits to the plasma membrane determine the biophysical states of Ca_V2.2 channels by regulating PIP₂ coupling to the nonspecific phospholipid-binding site in the I–II loop.