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Data suggest that c-Fos (proto-oncogene protein c-fos; not c-Jun) regulates phospholipid synthesis in cell nucleus; c-Fos localizes to nucleus and modulates genetic transcription through activation of Pip5k1.
optimal PIP5KIgamma (show PIP5K1C Proteins) and PI(4,5)P(2) expression, by osteoclasts, are essential for skeletal homeostasis
Our findings suggest that PI4P5Kalpha plays a complex role in restricting insulin release from pancreatic beta-cells through helping to maintain plasma membrane PIP(2) levels and integrity of the actin cytoskeleton under both basal and stimulatory conditions.
The results suggested that PIP5K1A (show PIP5K1B Proteins) and PIP5K1B (show PIP5K1B Proteins) may coordinately and/or redundantly function in the maintenance of sperm number and morphology during spermatogenesis.
findings indicate that synthesis of phosphatidylinositol 4,5-bisphosphate (PIP2) by the three phosphatidylinositol 4-phosphate 5-kinase (show PIP4K2C Proteins) (PIP5K (show PIKFYVE Proteins)) isoforms Ialpha, Ibeta and Igamma is controlled by Rho GTPases
that membrane turnover events regulating ENaC (show SCNN1A Proteins) surface expression and activity in oocytes and CCD (show RUNX2 Proteins) cells can be regulated by PI5KIalpha.
after stimulation of a G protein-coupled receptor (show GPR34 Proteins), IP(3) is completely derived from a rapidly synthesized discrete pool of PIP(2) synthesized by PIP5KIalpha (show PIP5K1B Proteins) and PIP5KIbeta (show PIP5K1B Proteins)
PIP5K (show PIKFYVE Proteins)-Ialpha may play an important role in both the proximal and distal steps of signaling cascade for insulin (show INS Proteins) secretion in beta-cells.
Blockade of IQGAP1 interaction with PIPKIalpha or PI(3 (show PI3 Proteins))K inhibited PtdIns(3,4,5)P3 generation and signalling, and selectively diminished cancer cell survival.
These results indicate that PP1 (show PPA1 Proteins) is recruited to the extracellular calcium-dependent E-cadherin (show CDH1 Proteins)-catenin-PIP5K1a complex in the plasma membrane to activate PIP5K1a, which is required for PLC (show HSPG2 Proteins)-g1 activation leading to keratinocyte differentiation.
PIP5K1A modulates ribosomal RNA gene silencing through its interaction with histone H3 (show HIST3H3 Proteins) lysine 9 trimethylation and heterochromatin protein HP1-alpha (show CBX5 Proteins).
PIP5K1A is modified by polySUMO-2 only during apoptosis.
CD28 (show CD28 Proteins) regulates phosphatidylinositol 4,5-biphosphate turnover by recruiting and activating phosphatidylinositol 4-phosphate 5-kinases alpha in human primary CD4 (show CD4 Proteins)(+) T lymphocytes.
Results define the role of PIPKI-alpha in cell migration and describes a new mechanism for the spatial regulation of Rac1 activity that is critical for cell migration.
Localized production of Phosphatidylinositol 4,5-bisphosphate by PIP5K1A is required for invadopodia formation by breast cancer cells.
Membrane ruffling requires coordination between this enzyme and Rac (show AKT1 Proteins) signaling.
in addition to its effects upon Rac activity, Ajuba can also influence cell migration through regulation of PI(4,5)P2 synthesis through direct activation of PIPKIalpha enzyme activity
identified apoptotic stimuli that initiate a signaling pathway during cell death that leads to caspase (show CASP3 Proteins)-independent downregulation of PIP5Kalpha.
Catalyzes the phosphorylation of phosphatidylinositol 4- phosphate (PtdIns4P) to form phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2). PtdIns(4,5)P2 is involved in a variety of cellular processes and is the substrate to form phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P3), another second messenger. The majority of PtdIns(4,5)P2 is thought to occur via type I phosphatidylinositol 4-phosphate 5-kinases given the abundance of PtdIns4P. Participates in a variety of cellular processes such as actin cytoskeleton organization, cell adhesion, migration and phagocytosis. Required for membrane ruffling formation, actin organization and focal adhesion formation during directional cell migration by controlling integrin-induced translocation of RAC1 to the plasma membrane. Together with PIP5K1C is required for phagocytosis, but they regulate different types of actin remodeling at sequential steps. Promotes particle ingestion by activating WAS that induces Arp2/3 dependent actin polymerization at the nascent phagocytic cup. Together with PIP5K1B is required after stimulation of G-protein coupled receptors for stable platelet adhesion. Plays a role during calcium-induced keratinocyte differentiation. Recruited to the plasma membrane by the E-cadherin/beta-catenin complex where it provides the substrate PtdIns(4,5)P2 for the production of PtdIns(3,4,5)P3, diacylglycerol and inositol 1,4,5-trisphosphate that mobilize internal calcium and drive keratinocyte differentiation. Together with PIP5K1C have a role during embryogenesis. Functions also in the nucleus where acts as an activator of TUT1 adenylyltransferase activity in nuclear speckles, thereby regulating mRNA polyadenylation of a select set of mRNAs.
phosphatidylinositol-4-phosphate 5-kinase type-1 alpha
, phosphatidylinositol-4-phosphate 5-kinase, type 1 beta
, phosphatidylinositol-4-phosphate 5-kinase, type I, alpha
, phosphatidylinositol-4-phosphate 5-kinase, type I, beta
, 68 kDa type I phosphatidylinositol 4-phosphate 5-kinase
, 68 kDa type I phosphatidylinositol-4-phosphate 5-kinase
, phosphatidylinositol 4-phosphate 5-kinase type I alpha
, phosphatidylinositol 4-phosphate 5-kinase type I beta
, phosphatidylinositol 4-phosphate 5-kinase type-1 alpha
, phosphatidylinositol-4-phosphate 5-kinase type I alpha
, phosphatidylinositol-4-phosphate 5-kinase type I beta
, ptdIns(4)P-5-kinase 1 alpha
, 68 kDa type I phosphatidylinositol 4-phosphate 5-kinase alpha
, 68 kDa type I phosphatidylinositol-4-phosphate 5-kinase alpha