PIP4K2C encodes phosphatidylinositol-5-phosphate 4-kinase type 2 gamma (PI5P4Kγ), a member of the type II phosphatidylinositol phosphate kinase family that catalyzes the conversion of phosphatidylinositol-5-phosphate into phosphatidylinositol-4,5-bisphosphate, thereby contributing to phosphoinositide metabolism and intracellular signaling regulation
[1]. Mechanistically, PIP4K2C participates in phosphatidylinositol-4,5-bisphosphate biosynthesis and has been linked to the negative regulation of insulin receptor signaling as well as the positive regulation of autophagosome assembly, placing this kinase at the interface of metabolic signaling and autophagy pathways
[1][2]. Experimental studies further demonstrate that deletion of Pip4k2c alters immune system regulation, supporting a broader role for PI5P4Kγ in cellular signaling networks beyond lipid metabolism
[3]. In disease-related models, PIP4K2C has attracted attention in cancer biology because suppression of its expression decreases intracellular PI(4,5)P
2 levels and inhibits proliferation, migration, and invasion of breast cancer cells while enhancing autophagic activity
[4]. Compared with the related isoforms PIP4K2A and PIP4K2B, PIP4K2C is distinguished by its relatively low enzymatic activity and has been proposed to function as a GTP-responsive kinase, highlighting isoform-specific regulatory properties within the PI5P4K family
[2]. For experimental applications, recent structural studies have reported crystal structures of PI5P4K2C bound to allosteric inhibitors, providing a framework for selective chemical probe development and mechanistic investigation of PIP4K2C-dependent signaling pathways
[2].