Phosphatidylinositol 5-phosphate 4-kinase (PIP4K) regulates TOR signaling and cell growth during Drosophila development

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PIP4Ks Suppress Insulin Signaling through a Catalytic-Independent Mechanism (2018, unknown): “As reported (Gupta et al., 2013), the loss of all three enzymes conferred a 2-fold increase in their substrate, PI(5)P (Figures 1C and 1D).”
In B cells, phosphatidylinositol 5-phosphate 4-kinase–α synthesizes PI(4,5)P2 to impact mTORC2 and Akt signaling (2016, background): “For example, stable knockout of Drosophila dPIP4K (orthologous to the highactivity PIP4K2A in higher species) results in a dramatic attenuation of Akt phosphorylation (20), whereas acute depletion of PIP4K2A in human leukocytes by RNAi results in increased Akt phosphorylation (19).”
Phosphatidylinositol-5-phosphate 4-kinases regulate cellular lipid metabolism by facilitating autophagy (2018, background): “Interestingly, the loss of function mutant of dPIP4K has a decrease in mTORC1 signaling (Gupta et al., 2013).”
Inhibition of PIP4Kγ ameliorates the pathological effects of mutant huntingtin protein (2017, methodology): “vation of PI5P cellular levels as previously described in the Drosophila mutant (Gupta et al., 2013).”
Deletion of the gene Pip4k2c, a novel phosphatidylinositol kinase, results in hyperactivation of the immune system (2016, background): “On the other hand, it was reported that knocking out the only PI5P4K isoform in Drosophila resulted in lower body weight and that this correlated with decreased mTORC1 signaling (7).”