Phosphatidylethanolamine (PE) (PE)

Phosphatidylethanolamine (PE) is a major structural glycerophospholipid that constitutes a significant fraction of mammalian cellular membranes, particularly in the brain and liver (Vance, 2015). It is characterized by its ability to promote negative membrane curvature, which is essential for processes such as membrane fusion, fission, and the completion of cytokinesis (Gibellini & Smith, 2010). Beyond its structural role, PE is a critical biochemical intermediate in the synthesis of phosphatidylcholine and serves as a substrate for the lipidation of LC3, a hallmark step in the formation of autophagosomes (Rockenfeller et al., 2015). In pathological conditions like cancer, PE is often externalized to the outer leaflet of the plasma membrane in tumor vascular endothelium, providing a specific site for targeted imaging and therapy (Stafford & Thorpe, 2011). Furthermore, the peroxidation of PE species containing polyunsaturated fatty acids is a primary driver of ferroptotic cell death, linking this lipid to neurodegeneration and acute organ injury (Kagan et al., 2017). Therapeutic agents such as duramycin exploit the unique binding pocket of the PE headgroup to exert antimicrobial effects or serve as molecular probes for detecting cell death and tumor vasculature (Zhao, 2011).

Other names

Cephalin1,2-diacyl-sn-glycero-3-phosphoethanolamineL-alpha-phosphatidylethanolamineGlycerophosphoethanolamine

Direct binding to the ethanolamine headgroup of the lipid, leading to membrane pore formation, inhibition of phospholipase A2, or disruption of autophagosome formation.