Phosphatidylinositolpolyphosphates (PtdInsPs) are centrally involved in many biologic processes, ranging from cell growth and organization of the actin cytoskeleton to endo- and exocytosis. PI4KII phosphorylates PtdIns at the D-4 position, an essential step in the biosynthesis of PtdInsPs. PI4K II is activated by detergent and inhibited by adenosine. Overexpression of PI4KII in COS-7 cells increases synthesis of PtdIns4P. Some cells overexpressing PI4KII have scattered or no perinuclear Golgi. Knockdown of PI4KII by RNA interference (RNAi) does not disrupt the Golgi, and some cells show expanded Golgi. RNAi reduces the Golgi level of PtdIns4P and blocks the association between AP1 and the trans-Golgi network. PI4KII RNAi had little effect on intra-Golgi trafficking, but it inhibited export to plasma membrane export by 35%. It has been proposed that PI4KII generates PtdIns4P-rich domains within the Golgi that specify docking of the AP1 coat machinery.
Phosphatidylinositol 4-kinase type 2-alpha; Phosphatidylinositol 4-kinase type II; phosphatidylinositol 4-kinase type II (PI4KII); Phosphatidylinositol 4-kinase type II-alpha; Type II alpha phosphatidylinositol 4-kinase