• PIPK I γ Polyclonal Antibody
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Upingbio

YP-Ab-14921-100UL

PIPK I γ Polyclonal Antibody

PIPK I γ Polyclonal Antibody

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  • Gene Name: PIP5K1C
  • Immunogen: The antiserum was produced against synthesized peptide derived from human PIP5K1C. AA range:305-354
  • Specificity: PIPK I γ Polyclonal Antibody detects endogenous levels of PIPK I γ protein.
  • Composition: Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
  • Source: Polyclonal, Rabbit,IgG
  • Dilution ratio: Western Blot: 1/500 - 1/2000. ELISA: 1/20000. Not yet tested in other applications.
  • Purification process: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
  • Concentration: 1 mg/ml
  • Storage: -20°C/1 year
  • Other Names: PIP5K1C; KIAA0589; Phosphatidylinositol 4-phosphate 5-kinase type-1 gamma; PIP5K1-gamma; PtdIns(4)P-5-kinase 1 gamma; Phosphatidylinositol 4-phosphate 5-kinase type I gamma; PIP5KIgamma
  • Background: phosphatidylinositol-4-phosphate 5-kinase type 1 gamma(PIP5K1C) Homo sapiens This locus encodes a type I phosphatidylinositol 4-phosphate 5-kinase. The encoded protein catalyzes phosphorylation of phosphatidylinositol 4-phosphate, producing phosphatidylinositol 4,5-bisphosphate. This enzyme is found at synapses and has been found to play roles in endocytosis and cell migration. Mutations at this locus have been associated with lethal congenital contractural syndrome. Alternatively spliced transcript variants encoding different isoforms have been described.[provided by RefSeq, Sep 2010],
  • Function: catalytic activity:ATP + 1-phosphatidyl-1D-myo-inositol 4-phosphate = ADP + 1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate.,disease:Defects in PIP5K1C are the cause of lethal congenital contractural syndrome type 3 (LCCS3) [MIM:611369]; also known as multiple contractural syndrome Israeli Bedouin type B. LCCS is an autosomal recessive disorder characterized by early fetal hydrops and akinesia, the Pena-Shokeir phenotype, specific neuropathology with degeneration of anterior horn neurons and extreme skeletal muscle atrophy. LCCS3 patients present at birth with severe multiple joint contractures with severe muscle wasting and atrophy, mainly in the legs. LCCS3 can be distinguished from the original LCCS by the absence of hydrops, fractures, and multiple pterygia.,enzyme regulation:Activated by interaction with TLN2.,function:Plays a role in membrane ruffling and assembly of clathrin-coate
  • Species: Human;Rat;Mouse;
  • Range: WB;ELISA
  • Protein: Phosphatidylinositol 4-phosphate 5-kinase type-1 gamma
  • DA: 80kD
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