Cloned (Comment) | Organism |
---|---|
FLAG-tagged PI4KIIIbeta is stably expressed in HEK-293 cells | Homo sapiens |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
PIK93 | - |
Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
endosome | isoozyme PI4KIIalpha | Homo sapiens | 5768 | - |
Golgi membrane | isozyme PI4KIIIbeta | Homo sapiens | 139 | - |
membrane | - |
Homo sapiens | 16020 | - |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Synonyms | Comment | Organism |
---|---|---|
phosphatidylinositol 4-kinase | - |
Homo sapiens |
PI4K | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | PI4KIIalpha knockdown causes enlarged LAMP-1-positive endosomal structures in fixed cells. Acute depletion of phosphatidylinositol 4-phosphate in the Golgi causes accumulation of LIMP-2 in this compartment, and PI4KIIIbeta is responsible for controlling the exit of LIMP-2 from the Golgi. In contrast, depletion of PI4KIIalpha blocks trafficking at a post-Golgi compartment, leading to accumulation of LIMP-2 in enlarged endosomal vesicles. PI4KIIalpha depletion also causes secretion of missorted GBA into the medium, which is attenuated by limiting LIMP-2/GBA exit from the Golgi by PI4KIIIbeta inhibitors, overview | Homo sapiens |
physiological function | distinct phosphatidylinositol 4-kinases play important roles at multiple steps in the trafficking pathway of the LIMP-2/GBA complex. The phosphatidylinositol 4-kinases control lysosomal delivery of the Gaucher disease enzyme, beta-glucocerebrosidase, overview. Catalytic activity of PI4KIIIbeta in Golgi exit of the LIMP-2/GBA complex, which is followed by PI4KIIalpha-mediated trafficking to lysosomes. PI4KIalpha is involved in post-Golgi trafficking of LIMP-2 along the degradative pathway | Homo sapiens |