Phosphatidylinositol 5-phosphate 4-kinase with low enzymatic activity. May be a GTP sensor, has higher GTP-dependent kinase activity than ATP-dependent kinase activity. PIP4Ks negatively regulate insulin signaling through a catalytic-independent mechanism. They interact with PIP5Ks and suppress PIP5K-mediated PtdIns(4,5)P2 synthesis and insulin-dependent conversion to PtdIns(3,4,5)P3. a 1,2-diacyl-sn-glycero-3-phospho-(1D-myo-inositol-5-phosphate) + ATP = a 1,2-diacyl-sn-glycero-3-phospho-(1D-myo-inositol-4,5-bisphosphate) + ADP + H(+) 1,2-dihexadecanoyl-sn-glycero-3-phospho-(1D-myo-inositol-5-phosphate) + ATP = 1,2-dihexadecanoyl-sn-glycero-3-phospho-(1D-myo-inositol-4,5-bisphosphate) + ADP + H(+) 1,2-dihexadecanoyl-sn-glycero-3-phospho-(1D-myo-inositol-5-phosphate) + GTP = 1,2-dihexadecanoyl-sn-glycero-3-phospho-(1D-myo-inositol-4,5-bisphosphate) + GDP + H(+) Interacts with PIP5K1A; the interaction inhibits PIP5K1A kinase activity. No significant expression was discerned throughout the prenatal brains except for the olfactory mantle zone, which exhibited the expression signals weakly. On P0 and P7, the expression was weakly positive in the gray matter throughout the brain, with higher expression in the olfactory mitral cell layer. In the cerebellum, the expression was evenly positive in external and internal granule cell layers. On P21 and P56, the expression in non-cortical brain parenchyma was negligible. However, the expression was evident in the olfactory mitral cell layer, the piriform cortex, the hippocampal pyramidal CA1-3, and the cerebellar Purkinje cell layer, although much less distinct in the dentate granule cell layer and the cerebellar granule cell layer. In the cerebral cortex, the expression was weaker in layer V than the other layers. No significant expression was seen in the white matter. Phosphorylated, phosphorylation is induced by EGF.