Cell Signaling Technology

Product Pathways - Ca / cAMP / Lipid Signaling

PIP4K2A (D83C1) Rabbit mAb #5527

No. Size Price
5527S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
5527 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey,Bovine,Pig, Endogenous 50 Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Homology

Species predicted to react based on 100% sequence homology: Dog, Horse,

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.

PIP4K2A (D83C1) Rabbit mAb兔单抗识别内源性水平的总磷脂酰肌醇 5-磷酸 4-激酶II 型alpha (PIP4K2A)蛋白。该抗体不与PIP4K2B或 PIP4K2C发生交叉反应,并且预计不与type I PIP5Ks或PIKfyve发生交叉反应。

Source / Purification

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

该单克隆抗体通过用合成肽免疫动物制备,该合成肽与人PIP4K2A蛋白靠近羧基末端的残基一样。

Western Blotting

Western Blotting

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

Western blot方法检测多个细胞系提取物,使用的抗体为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).

磷脂酰肌醇 5-磷酸 4-激酶II 型alpha (PtdIns 4-Kinase type II alpha, PIP4K2A)是三个已知的II型磷脂酰肌醇激酶家族之一,包括PIP4K2A, PIP4K2B和PIP4K2C。每种激酶都可以催化5-单磷酸磷脂酰肌醇(PI5-P)磷酸化,形成4,5 - 二磷酸磷脂酰肌醇(PI4,5-P2)。PIP4K2A最初被认为是一个PI4-P5-激酶(1,2),之后,显示PIP4K2A 可以使PI5-P的4-位磷酸化,从而将其定义为一个新的脂质激酶家族(3)。在大脑中,PIP4K2A以最高水平广泛表达,已经在精神分裂症患者和其他神经元疾病患者中发现PIP4K2A突变(4-8)。PI 5-P的变化水平显著地响应于生理和病理性刺激(5-12),与核仁磷酸蛋白变性淋巴瘤酪氨酸激酶的细胞转化一样(13)。与此相反,低渗休克和组胺会降低PI5-P的细胞水平(14,15)。在响应DNA损伤和细胞应激中,PIP4K2A在抑制有丝分裂原依赖性的PI5-P增加过程中发挥重要作用(16-18)。PIP4K2A通过将PI 5-P转化为PI 4,5-P2来调节PI 5-P的水平,从而防止PI 5-P与ING2相互作用并调节ING2活性来激活p53和p53依赖的凋亡信号通路(19)。已经显示,PIP4K2A与PIP4K2B形成异二聚体,导致招募到细胞核。有趣的是,由此推论,PIP4K2A的活性是PIP4K2B的2000倍,表明这两个脂激酶串联起作用,PIP4K2B作为靶向亚基和PIP4K2A作为催化组分(18)。PIP4Ks同样可能在脂囊泡形成和/或高尔基体内稳态中起作用(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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