The C2-domain of cytoplasmic phospholipase A₂α is structurally designed to target PC-rich membrane regions to increase the enzymatic efficiency of the catalytic domain, which prefers PCs with polyunsaturated acyl chains.

Phosphatidic acid regulates recycling of endocytosed plasma membrane vesicles in polarized cells through a retromer and Arf1 dependent process.

GDE3 is a transmembrane GPI-specific phospholipase C that sheds the urokinase receptor (uPAR) from the cell surface resulting in loss of uPAR function in breast cancer cells and reduced tumor growth.

T cell receptor signaling is regulated by newly polymerized F-actin foci at the immunological synapse.

SAA removes toxic products of lipolysis of the cell membrane by sPLA₂, indicating that SAA and sPLA₂ act synergistically to clear debris from injured sites, as required for tissue healing.

β-adrenergic receptors at the Golgi apparatus activate a local signaling pathway, not accessed by cell surface receptors, to drive cardiac hypertrophy and could represent a target for heart failure therapy.

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

Sec14l3/SEC14L2 respond to upstream Wnt/Frizzled/Dvl stimulation to recruit and activate phospholipase Cδ4a (Plcδ4a) to further initiate calcium release.

Tannic acid acts as an ‘antidote’ against the negative effects of a bacterial enzyme, which can both aggravate cystic fibrosis and enable the anthrax bacteria to evade the immune responses elicited by a typical live vaccine.

Considering the course of a pathogen's evolution, there appears to be interplay between secretion systems, providing unique, synergistic mechanisms to support a successful lifestyle for possibly pathogenesis, symbiosis and/or parasitosis.