Cell Signaling Technology

Product Pathways - Ca / cAMP / Lipid Signaling

PIP4K2A (D83C1) Rabbit mAb #5527

Applications Reactivity Sensitivity MW (kDa) Isotype
W H M R Mk B Pg (Dg) (Hr) Endogenous 50 Rabbit IgG

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  B=Bovine  Dg=Dog  Pg=Pig  Hr=Horse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

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.

Source / Purification

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

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using PIP4K2A (D83C1) Rabbit mAb.

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.

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