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The polarity protein crumbs controls apical secretion and the architecture of the apical domain by modulating PI(4,5)P₂ levels and the organization of apical Rab6-, Rab11-, and Rab30-dependent trafficking.

Molecular dynamics simulations reveal the formation of membrane pores by gasdermin-D, the ultimate effector of pyroptotic cell death in inflammation and infection.

A genome editing resource for discovering, in Drosophila, the organization of cellular structure and function by phosphoinositide signaling.

The high-resolution X-ray crystal structure of PLC-γ1 reveals a unifying model for the regulation of the PLC-γ isozymes.

A dual-color TIRFM study reveals a new form of inflammatory regulation, in which a lipid kinase and ion channel reciprocally regulate each other to amplify the response to painful stimuli.

The local PI(4,5)P₂ nanodomain promotes the dimerization and activation of EGFR in the plasma membrane, whereas activated EGFR dissolves the nanodomain structure of PI(4,5)P₂ through PLCγ.

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 first reconstitution of an unconventional secretory mechanism uncovered the molecular mechanism by which Fibroblast Growth Factor 2 is secreted from mammalian cells.

The kinase AKT acts as a nodal point that coordinates both positive and negative cues to regulate the regeneration of central nervous system axons in adult mice.

Multiple dynamic protein interactions converge to regulate the catalytic activity of the B cell kinase, BTK.