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Human Phosphatidylinositol 4-Kinase, Catalytic, alpha (PI4KA) interaction partners

1. Architecture of the human PI4KIIIalpha lipid kinase complex.

2. hCKalpha functions as an indispensable regulator that bridges PI4KIIIalpha and hepatitis C virus NS5A and potentiates NS5A-stimulated PI4KIIIalpha activity, which then facilitates the targeting of the ternary complex to the endoplasmic reticulum for viral replication.

3. Blockade of IQGAP1 interaction with PIPKIalpha or PI(3)K inhibited PtdIns(3,4,5)P3 generation and signalling, and selectively diminished cancer cell survival.

4. The results showed that, in contrast to the enteroviruses and the cardioviruses, foot-and-mouth disease virus replication does not require PI4KIII (PI4KIIIalpha and PI4KIIIbeta), and phosphatidylinositol 4-phosphate levels do not increase in foot-and-mouth disease virus-infected cells and phosphatidylinositol 4-phosphate is not seen at replication organelles.

5. Missense mutations in PI4KA are associated with perisylvian polymicrogyria, cerebellar hypoplasia and arthrogryposis.

6. Our results suggest a plasticity of the molecular interactions that control PI4KIIIalpha localization and functions at the plasma membrane.

7. PI4K III alpha plays a role in biosynthetic trafficking of two different classes of proteins from the ER to the Golgi complex.

8. PI4KA and GRM3 polymorphisms have potential to jointly modulate antipsychotic response

9. our results suggest a mechanism of PI4K IIalpha recruitment, regulation, and function at the membrane.

10. These results suggest that type II PtdIns 4-kinases are part of piperine-mediated anti-inflammatory signaling mechanisms

11. The N-terminal 1,152 amino acids were dispensable for hepatitis C virus replication, phosphatidylinositol 4-phosphate induction, and enzymatic function, thereby defining the minimal PI4KIIIalpha core enzyme at a size of ca. 108 kDa.

12. PI4KA mRNA could be used as a new molecular marker to improve established prognostic models for hepatocellular carcinoma.

13. Descriptive Statement The genetic interactions associated with ILVatrophy rate in this study may be mapping variants inSYNJ2andPI4KAthat interact to decrease synthesisof PIP.

14. PI4KA is essential for the maintenance of plasma membrane phosphatidylinositol 4,5-bisphosphate pools but only during strong stimulation of receptors coupled to phospholipase C activation.

15. we demonstrate that PI4KIIIalpha activity affects the NS5A phosphorylation status.

16. Cell culture studies with Phosphatidylinositol-4-kinase IIIalpha inhibitors demonstrated that the kinase activity was essential for hepatitis C virus RNA replication.

17. Phosphatidylinositol 4-kinase IIalpha is palmitoylated by Golgi-localized palmitoyltransferases in cholesterol-dependent manner

18. PI4KA is necessary for the local enrichment of PI 4-phosphate at the hepatitis c virus membranous web.

19. These results suggest that hepatitis C virus NS5A modulation of PI4KA-dependent phosphatidylinositol 4-phosphate production influences replication complex formation.

20. confirmed the high copy number of PI4KIIIalpha transcript in K562 cells along with several genes located in the same region in Chr22, including two pseudogenes that cover most exons coding for isoform 1, consistent with chromosome amplification

Mouse (Murine) Phosphatidylinositol 4-Kinase, Catalytic, alpha (PI4KA) interaction partners

1. PI4KA is essential for the maintenance of plasma membrane phosphatidylinositol 4,5-bisphosphate pools but only during strong stimulation of receptors coupled to phospholipase C activation.

2. It was shown that PI4KIIIalpha was targeted to the plasma membrane as part of an evolutionarily conserved complex containing Efr3/rolling blackout, which was found to be a palmitoylated peripheral membrane protein.

3. Loss of phosphatidylinositol 4-kinase 2alpha activity causes late onset degeneration of spinal cord axons.