Cell Signaling Technology

Product Pathways - MAPK Signaling

DUSP4/MKP2 (D9A5) Rabbit mAb #5149

No. Size Price
5149S 100 µl ( 10 western blots ) ¥3,250.00 现货查询 购买询价 防伪查询
5149 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Monkey, Endogenous 42 Rabbit

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

DUSP4/MKP2 (D9A5) Rabbit mAb recognizes endogenous levels of total DUSP4 protein.

DUSP4/MKP2 (D9A5)Rabbit mAb可以识别内源性的总DUSP4蛋白。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro168 of human DUSP4 protein.


Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using DUSP4/MKP2 (D9A5) Rabbit mAb (upper) or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower).使用DUSP4/MKP2 (D9A5)Rabbit mAb(上)或GAPDH (D16H11) XP®Rabbit mAb#5174(下)对多种细胞提取物进行western blot分析。


MAP kinases are inactivated by dual-specificity protein phosphatases (DUSPs) that differ in their substrate specificity, tissue distribution, inducibility by extracellular stimuli, and cellular localization. DUSPs, also known as MAPK phosphatases (MKP), specifically dephosphorylate both threonine and tyrosine residues in MAPK P-loops and have been shown to play important roles in regulating the function of the MAPK family (1,2). At least 13 members of the family (DUSP1-10, DUSP14, DUSP16, and DUSP22) display unique substrate specificities for various MAP kinases (3). MAPK phosphatases typically contain an amino-terminal rhodanese-fold responsible for DUSP docking to MAPK family members and a carboxy-terminal catalytic domain (4). These phosphatases can play important roles in development, immune system function, stress responses, and metabolic homeostasis (5). In addition, research studies have implicated DUSPs in the development of cancer and the response of cancer cells to chemotherapy (6).

MAPK能被双特异性蛋白磷酸酶(DUSPs)失活,DUSPs由其不同的底物、组织分布、细胞外刺激的诱导性和细胞内定位而不同。DUSPs,也被称为MAPK磷酸酶(MKP),能够特异性的去磷酸化MAPK P-loops的苏氨酸和酪氨酸残基,在调控MAPK家族功能的过程中发挥了重要作用(1,2)。已经发现了至少13个成员(DUSP1-10, DUSP14, DUSP16和DUSP22),针对多种MAPK展现了独特的底物特异性(3)。MAPK磷酸酶含有典型的氨基端rhodanese-fold以便DUSP与MAPK家族成员结合,和一个羧基端催化结构域(4)。这些磷酸酶在发育、免疫系统功能、压力应激和代谢稳态过程中发挥了重要作用(5)。此外,研究提示DUSPs涉及了癌症发展和癌细胞对化疗的反应(6)。

DUSP4 (MKP2, hVH2) is a nuclear dual-specificity phosphatase that is a negative regulator of Erk1/2 signaling by dephosphorylating and inactivating Erk1/2 in response to growth factors (7,8). Treatment with mitogen or expression of activating mutations of Ras (G12V) or Raf (V600E) promote increased expression of DUSP4 and a coincident decrease in phospho-Erk in the nucleus (9). In contrast, numerous studies have detected decreased expression of DUSP4 in a variety of tumor types, resulting in increased signaling via the Ras/Erk pathway, enhanced tumor growth, and decreased drug sensitivity (10-12). DUSP4/MKP2 also plays an important role in regulating the immune system where it has been implicated in regulating T and B cell proliferation and apoptosis, and adaptive and inflammatory responses (13-16).

DUSP4 (MKP2, hVH2)是一个细胞核双特异性磷酸酶,是Ekr1/2信号的负调因子,可以在生长因子的作用下去磷酸化并失活Erk1/2(7,8)。使用有丝分裂原或表达突变激活型的Ras(G12V)或Raf (V600E)能够促进DUSP4的表达随之减少细胞核中磷酸化的Erk(9)。相应的,多种研究发现DUSP4在多种肿瘤中表达下降,导致Ras/Erk信号加强,促进肿瘤生长,降低对药物的敏感性(10-12)。DUSP4/MKP2也在调控免疫系统的过程中发挥了重要作用,提示它能调控T和B细胞扩增和凋亡,适应性和炎症反应(13-16)。

  1. Camps, M. et al. (2000) FASEB J 14, 6-16.
  2. Theodosiou, A. and Ashworth, A. (2002) Genome Biol 3, REVIEWS3009.
  3. Salojin, K. and Oravecz, T. (2007) J Leukoc Biol 81, 860-9.
  4. Tanoue, T. et al. (2002) J Biol Chem 277, 22942-9.
  5. Dickinson, R.J. and Keyse, S.M. (2006) J Cell Sci 119, 4607-15.
  6. Wu, G.S. (2007) Cancer Metastasis Rev 26, 579-85.
  7. Peng, D.J. et al. (2010) Cell Cycle 9, 4650-5.
  8. Lawan, A. et al. (2011) J Biol Chem 286, 12933-43.
  9. Cagnol, S. and Rivard, N. (2012) Oncogene , .
  10. Chitale, D. et al. (2009) Oncogene 28, 2773-83.
  11. Waha, A. et al. (2010) Cancer Res 70, 1689-99.
  12. Balko, J.M. et al. (2012) Nat Med 18, 1052-9.
  13. Ramesh, S. et al. (2008) EMBO Rep 9, 990-7.
  14. Cornell, T.T. et al. (2010) Infect Immun 78, 2868-76.
  15. Huang, C.Y. et al. (2012) Eur J Immunol 42, 476-88.
  16. Yu, M. et al. (2012) Proc Natl Acad Sci U S A 109, E879-88.

Application References

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