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These results indicate that GABARAP and PI4K2A interact tightly. Although lipidation of GABARAP is essential for its role in autophagy, here we show that its lipidation is not required for the interaction of GABARAP and PI4K2A.
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PI-273 is the first substrate-competitive, subtype-specific inhibitor of PI4KIIalpha, the use of which will facilitate evaluations of PI4KIIalpha as a cancer therapeutic target.
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Mining oncogenomic databases revealed that loss of the PI4K2B allele and underexpression of PI4KIIbeta mRNA are associated with human cancers. This finding supports the cell data and suggests that PI4KIIbeta may be a clinically significant suppressor of invasion.
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RNA interference of the type II phosphatidylinositol 4-kinases PI4KIIa and PI4KIIa in primary human endothelial cells leads to formation of an increased proportion of short WPB with perturbed packing of VWF, as exemplified by increased exposure of antibody-binding sites.
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PtdIns4KIIalpha regulates receptor sorting at early endosomes through a PtdIns(4)P-dependent pathway and contributes substrate for the synthesis of endosomal PtdIns(4,5)P2.
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Here two crystal structures are presented: the structure of human PIK42A and the structure of PIK42B containing a nucleoside analogue.
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PI4KIIalpha is a specific downstream effector of GABARAP and it generates PI4P, which has a key role in the final stage of autophagy.
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phosphatidylinositol 4-kinase IIalpha knockdown inhibited vesicle-associated membrane protein 3 trafficking to perinuclear membranes and impaired the rate of VAMP3-mediated recycling of the transferrin receptor
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structure and phylogenetic analysis
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PI4K2A is a novel regulator of vesicular trafficking and neurotransmission in the brain.
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The palmitoylation insertion contributes to the phosphatidylinositol-binding pocket and anchors PI4KIIalpha to the membrane.
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The Hermansky-Pudlak syndrome complex BLOC-1 and its cargo PI4KIIalpha interact with regulators of the actin cytoskeleton.
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Knockdown of PI4KIIalpha inhibits EGF-stimulated Akt phosphorylation.
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Results suggest that the phosphatidylinositol 4-kinase 2-alpha gene may not be a cause of autosomal recessive hereditary spastic paraplegia in humans.
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PI4KIIalpha is a novel regulator of tumor growth by its action on angiogenesis and HIF-1alpha regulation.
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Association of T cell antigen CD7 with type II phosphatidylinositol-4 kinase, a key component in pathways of inositol phosphate turnover.
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The active site of this enzyme occurs in a p97/valosin-containing-protein-rich fraction of the endoplasmic reticulum
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propose that PI4KIIalpha establishes the Golgi's unique lipid-defined organelle identity by generating PI(4)P-rich domains that specify the docking of the AP-1 coat machinery
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The linkage of CD63 with PI 4-kinase type II may result in the recruitment of this signaling enzyme to specific membrane locations in the platelet where it influences phosphoinositide-dependent signaling and platelet spreading.
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changes in membrane environment can regulate PI4KIIalpha activity.
