site-directed mtagenesis, mutation of the putative ATP and 1-phosphatidyl-1D-myo-inositol 4-phosphate binding site, cells form extremely extended bipolar neurits even in presence of serum, failed to interfere with cell flattening and neurite extension
the mutations of PIP5Kalpha decreases the substrate affinity and the enzyme efficiency for 1-stearoyl-2-arachidonoyl phosphatidylinositol-4-phosphate compared to the wild-type enzyme
the mutations of PIP5Kalpha decreases the substrate affinity and the enzyme efficiency for 1-stearoyl-2-arachidonoyl phosphatidylinositol-4-phosphate compared to the wild-type enzyme
site-directed mutagenesis, overexpression of the catalytically inactive construct of isozyme gamma splicing form c in rat cerebellar granule cells causes progressive loss of their neuronal processes, not observed with expression of isozyme gamma splicing form a
site-directed mutagenesis, overexpression of the catalytically inactive construct of isozyme gamma splicing form c in rat cerebellar granule cells causes progressive loss of their neuronal processes, not observed with expression of isozyme gamma splicing form a
mutant plants homozygous for T-DNA-disrupted PIP5K3 alleles are compromised in root hair formation. Root hair-specific PIP5K3 overexpression results in root hair deformation and loss of cell polarity with increasing accumulation of PIP5K3 transcript. An N-terminal domain containing membrane occupation and recognition nexus repeats, which is not required for catalytic activity, is essential for the establishment of root hair growth. Transient heterologous expression of full-length PIP5K3 in Nicotiana tabacum pollen tubes increases plasma membrane association of a phosphatidylinositol 4,5-bisphoshate-specific reporter
overexpression of isoform PPK-1 in Caenorhabditis elegans causes an increase in 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate levels in vivo. In developing neurons, PPK-1 overexpression leads to growth cones that become stalled, produce ectopic membrane projections, and branched axons. Once neurons are established, PPK-1 overexpression results in progressive membrane overgrowth and degeneration during adulthood
overexpression of isoform PPK-1 in Caenorhabditis elegans causes an increase in 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate levels in vivo. In developing neurons, PPK-1 overexpression leads to growth cones that become stalled, produce ectopic membrane projections, and branched axons. Once neurons are established, PPK-1 overexpression results in progressive membrane overgrowth and degeneration during adulthood
chimeric protein in which the core kinase domain of phosphatidylinositol 4-phosphate 5-kinase 1alpha has been fused to a beta-arrestin mutant deficient in phosphatidylinositol 4,5-bisphosphate binding rescues internalization of beta2-adrenergic receptor
knockdown of phosphatidylinositol 4-phosphate 5-kinase beta with siRNA inhibits cell polarization and impairs cell directionality during dHL60 chemotaxis
PIP5Kgamma isozyme knockout by siRNA. Transfection of HK2 cells with PIP5Kgamma siRNA prevents advanced glycation end products-bovine serum albumin inhibition of renal Na+/K+ ATPase activity
construction of N-terminal deletion mutants DELTA68, DELTA 72, and DELTA74 are still localized to the plasma membrane, while the N-terminal deletion mutants DELTA82, DELTA 97 are mislocated to the cytosol, construction of C-terminal deletion mutant DELTA446 is still localized to the plasma membrane, while the N-terminal deletion mutant DELTA444 is mislocated to the cytosol, mutant fusion protein DELTA68-DELTA444 localizes to the plasma membrane
expression of phosphatidylinositol 4-phosphate 5-kinase alpha in Xenopus laevis oocytes decreases epithelial sodium channel currents by 80%, entirely due to a decrease in cell surface epithelial sodium channel levels. Expression of catalytically inactive mutants has no effect on epithelial sodium channel activity. Knock-down of phosphatidylinositol 4-phosphate 5-kinase alpha with isoform-specific siRNA results in a 4fold enhancement of epithelial sodium channel activity
PIP5Kgamma isozyme knockout by siRNA. Transfection of HK2 cells with PIP5Kgamma siRNA prevents advanced glycation end products-bovine serum albumin inhibition of renal Na+/K+ ATPase activity