Phosphatidylinositol 4,5-bisphosphate

Phosphatidylinositol 4,5-bisphosphate (L-alpha-Phosphatidylinositol-4,5-bisphosphate) (10-25 μM, endogenous levels; 200-400 s, 250 s) and its water-soluble analog diC8-PI(4,5)P₂ maintain the conductive state of wild-type mouse ANO1 channels in HEK cells by preventing Ca²⁺-induced inactivation and rescuing channel activity after PI(4,5)P₂ depletion^[2].
Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P₂) (10 μM) binds to specific residues in multiple sites on mouse ANO1 channels to regulate channel gating and prevent Ca²⁺-induced inactivation, with mutations in these sites eliminating or reducing PI(4,5)P₂ sensitivity^[2].
Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P₂) modulates the conformation of mouse ANO1 channels by inducing TM6 rotation, which prevents Ca²⁺-induced pore collapse and maintains the conductive channel state^[2].
Phosphatidylinositol 4,5-bisphosphate constitutes 1-2 mol^% of total mammalian plasma membrane lipid, with a specific stearic acid-arachidonic acid acyl chain profile, and is the most abundant cellular phosphoinositide^[3].
Phosphatidylinositol 4,5-bisphosphate acts as a substrate for mammalian PLC isoforms, whose hydrolysis produces the second messengers IP₃ and DAG to drive downstream Ca²⁺ and PKC signaling^[3].
Phosphatidylinositol 4,5-bisphosphate dynamically regulates mammalian actin cytoskeleton dynamics by modulating the activity and localization of actin-binding proteins, including ERM proteins, cofilin, and N-WASP, with PLC-mediated PI(4,5)P₂ depletion driving actin disassembly and cell migration in carcinoma cells^[3].
Phosphatidylinositol 4,5-bisphosphate is essential for multiple steps of mammalian clathrin-mediated endocytosis, including AP2 activation, clathrin recruitment, membrane deformation, dynamin-mediated scission, and regulation of vesicle uncoating via localized production and degradation^[3].
Phosphatidylinositol 4,5-bisphosphate directly regulates the activity and localization of multiple mammalian plasma membrane ion channels, maintaining Kir and KCNQ channels in an open state, inhibiting TRPV4 channels, and contributing to GABA_A receptor membrane localization, with PLC-mediated PI(4,5)P₂ depletion dynamically altering channel activity^[3].
Phosphatidylinositol 4,5-bisphosphate forms nanoscale clusters (~65-73 nm) in the mammalian plasma membrane, with a portion bound to cytoskeletal proteins, and its local enrichment is regulated by lipid raft trapping, protein sequestration, and localized synthesis^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.