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Description :Recombinant full-length human PIP5K1C was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag.
Tag :GST tag
Expression System:Sf9 insect cells using baculovirus
Sequence :Full length
Genbank Number :NM_012398
Specific Activity :Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability, and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Applications :Kinase Assay
Molecular Weight :120 kDa
Gene Aliases :KIAA0589; LCCS3; PIP5K-GAMMA; PIP5Kgamma; PIPKIg_v4
Scientific Background :PIP5K1C or phosphatidylinositol-4-phosphate 5-kinase 1 gamma phosphorylates phosphatidylinositol-4-phosphate to form phosphatidylinositol 4,5-bisphosphate. PIP5K1C is found at synapses and has been found to play roles in endocytosis and cell migration. PIP5K1C directly associates with β-catenin and increases β-catenin activity downstream of growth factor stimulation (1). PIP5K1C expression and kinase activity enhance β-catenin phosphorylation on residues that promote nuclear importation and transcriptional activity. PIP5K1C deficiency impairs neutrophil recruitment as a result of defect in adhesion. PIP5K1C regulated the adhesion through facilitating RhoA GTPase and integrin activation by chemoattractants (2).
1. Schramp M. et al: PIPKIγ regulates β-catenin transcriptional activity downstream of growth factor receptor signaling. Cancer Res. 2011 Feb 15;71(4):1282-91.
2. Xu W, Integrin-induced PIP5K1C kinase polarization regulates neutrophil polarization, directionality, and in vivo infiltration. Immunity. 2010 Sep 24;33(3):340-50.
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Research Areas :AKT/PKB Pathway, Angiogenesis, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Inflammation, Invasion/Metastasis, Lipid Kinases, Metabolic Disorder, Neurobiology, NfkB Pathway, WNT Signaling