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Render Timestamp: 2024-10-09T09:43:26.764Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
  1. Products /
  2. Primary Antibodies /
  3. PIP4K2A (D83C1) Rabbit mAb
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

PIP4K2A (D83C1) Rabbit mAb #5527

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R Mk B Pg
    SENSITIVITY Endogenous
    MW (kDa) 50
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 
    • B-Bovine 
    • Pg-Pig 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    PIP4K2A (D83C1) Rabbit mAb recognizes endogenous levels of total PI 5-P 4-kinase type-2 alpha (PIP4K2A) protein. This antibody does not cross-react with PIP4K2B or PIP4K2C and is not predicted to cross-react with type I PIP5Ks or PIKfyve.

    Species Reactivity:

    Human, Mouse, Rat, Monkey, Bovine, Pig

    The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

    Species predicted to react based on 100% sequence homology:

    Dog, Horse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human PIP4K2A protein.

    Background

    Phosphatidylinositol 5-phosphate 4-kinase type-2 alpha (PtdIns 4-Kinase type II alpha, PIP4K2A), is one of three known members of the type II PIP kinase family, consisting of PIP4K2A, PIP4K2B, and PIP4K2C. Each catalyzes the phosphorylation of phosphatidylinositol 5-monophosphate (PI 5-P) to form phosphatidylinositol 4,5-bisphosphate (PI 4,5-P2). Originally thought to be a PI 4-P 5-Kinase (1,2), PIP4K2A was subsequently shown to phosphorylate the 4-position of PI 5-P, thus defining a new family of lipid kinases (3). Ubiquitously expressed with highest levels in the brain, mutations in PIP4K2A have been described in patients with Schizophrenia and other neuronal disorders (4-8).

    The levels of PI 5-P change significantly in response to physiological and pathological stimuli (5-12), as well as cell transformation with nucleophosmin anaplastic lymphoma tyrosine kinase (13). In contrast, hypoosmotic shock and histamine decrease cellular levels of PI 5-P (14,15). PIP4K2A has been hypothesized to play a role in suppressing mitogen-dependent increases in PI 5-P in response to DNA damage and cellular stress (16-18). PIP4K2A regulates the levels of PI 5-P in the nucleus by converting the PI 5-P to PI 4,5-P2, thus preventing PI 5-P from interacting with and regulating the ability of ING2 to activate p53 and p53-dependent apoptotic pathways (19). PIP4K2A has been shown to form a heterodimer with PIP4K2B resulting in its recruitment to the nucleus. Interestingly, PIP4K2A is 2000-fold more active than PIP4K2B in this context, suggesting that the two lipid kinases act in tandem, with PIP4K2B acting as the targeting subunit and PIP4K2A the catalytic component (18). PIP4Ks may also play a role in lipid vesicle formation and/or Golgi homeostasis (20).
    1. Divecha, N. et al. (1995) Biochem J 309 ( Pt 3), 715-9.
    2. Boronenkov, I.V. and Anderson, R.A. (1995) J Biol Chem 270, 2881-4.
    3. Rameh, L.E. et al. (1997) Nature 390, 192-6.
    4. Stopkova, P. et al. (2003) Am J Med Genet B Neuropsychiatr Genet 123B, 50-8.
    5. Schwab, S.G. et al. (2006) Mol Psychiatry 11, 837-46.
    6. Bakker, S.C. et al. (2007) Genes Brain Behav 6, 113-9.
    7. Fedorenko, O. et al. (2008) Psychopharmacology (Berl) 199, 47-54.
    8. Salazar, G. et al. (2009) J Biol Chem 284, 1790-802.
    9. Morris, J.B. et al. (2000) FEBS Lett 475, 57-60.
    10. Sbrissa, D. et al. (2004) Endocrinology 145, 4853-65.
    11. Guittard, G. et al. (2009) J Immunol 182, 3974-8.
    12. Sarkes, D. and Rameh, L.E. (2010) Biochem J 428, 375-84.
    13. Coronas, S. et al. (2008) Biochem Biophys Res Commun 372, 351-5.
    14. Sbrissa, D. et al. (2002) J Biol Chem 277, 47276-84.
    15. Roberts, H.F. et al. (2005) FEBS Lett 579, 2868-72.
    16. Doughman, R.L. et al. (2003) J Membr Biol 194, 77-89.
    17. Wilcox, A. and Hinchliffe, K.A. (2008) FEBS Lett 582, 1391-4.
    18. Bultsma, Y. et al. (2010) Biochem J 430, 223-35.
    19. Gozani, O. et al. (2003) Cell 114, 99-111.
    20. De Matteis, M.A. et al. (2005) Biochim Biophys Acta 1744, 396-405.

    Database Links

    UniProt ID: P48426


    Entrez-Gene Id: 5305


    Limited Uses

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    For Research Use Only. Not For Use In Diagnostic Procedures.
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