EC Number   |
General Information |
Reference |
|---|
   2.7.1.67 | evolution |
in vertebrates, PtdIns4P is synthesized by four distinct PI4K enzymes that belong to either the type-II or type-III family, each having alpha- and beta-forms. The type-III PI4Ks are relatives of the PI 3-kinase family, while the smaller type-II enzymes form a separate family |
721713 |
| 2.7.1.67 | malfunction |
an enzyme-deficient mutant displays defects in vegetative growth, deoxynivalenol production and pathogenicity. Furthermore, the deletion mutant also exhibits increased resistance to osmotic (NaCl, KCl and sorbitol), oxidative (H2O2) and cell wall (Congo Red and SDS) stresses |
-, 759289 |
| 2.7.1.67 | malfunction |
an enzyme-deficient mutant presents serrated leaves, which is resulted from the accelerated cell division and increased auxin concentration at serration tips |
760009 |
| 2.7.1.67 | malfunction |
depletion of PI4KIIalpha by siRNA-mediated knockdown reduces Wnt5a-triggered uptake and/or sorting of Fz4-eGFP into EEA1-positive endosomes. This effect is fully rescued by re-expression of siRNA-resistant PI4KIIalpha |
722121 |
| 2.7.1.67 | malfunction |
depletion of PIK1 results in a subsequent loss of intracellular 1-phosphatidyl-1D-myo-inositol 4-phosphate, and loss of Pik1 induces elongated growth, because knockdown of PIK1 results in the constitutive activation of Kss1, which subsequently drives elongated growth |
722704 |
| 2.7.1.67 | malfunction |
downregulation of enzyme expression negatively affects chilli leaf curl virus pathogenesis in Nicotiana benthamiana |
759796 |
| 2.7.1.67 | malfunction |
enzyme knockdown of isoform PI4KIIalpha -but not PI4KIIbeta - impairs toll-interleukin 1 receptor domain-containing adaptor protein and toll-like receptor 4 localization to phagosomes, reduces proinflammatory cytokine secretion, abolishes phagosomal tubule formation, and impairs major histocompatibility complex II presentation |
760073 |
| 2.7.1.67 | malfunction |
hepatitis C virus, by recruiting PI4KIIIa in the RNA replication complex, hijacks phosphatidylinositol-4 phosphate metabolism, ultimately resulting in a markedly altered subcellular distribution of the PI4KIIIalpha product. Antiviral effect of 4-anilino quinazoline compounds is mediated by the inhibition of PI4KIIIalpha and the consequent depletion of 1-phosphatidyl-1D-myo-inositol 4-phosphate required for the HCV membranous web. Inhibition of PI4KIIIalpha by AL-9 induces the formation of large viral NS5A protein clusters |
723609 |
| 2.7.1.67 | malfunction |
in PI4KII mutants, mucin-containing glue granules fail to reach normal size, with glue protein aberrantly accumulating in enlarged Rab7-positive late endosomes. PI4KIIDELTA mutants reveal small glue granules of grossly normal morphology, PI4KIIDELTA cells also exhibited large vacuolated structures not observed in wild-type, phenotype, overview. Retromer localization and dynamics are altered in PI4KIIDELTA mutants |
722098 |
| 2.7.1.67 | malfunction |
Inhibitors of phosphatidylinositol 4-phosphate synthesis or depletion of PI4KIIIalpha, a phosphatidylinositol 4-kinase localized to the endoplasmic reticulum and Golgi, prevents the recruitment of GBF1 to Golgi membranes |
722857 |
