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Gene Review

Map3k2  -  mitogen-activated protein kinase kinase...

Mus musculus

Synonyms: 9630061B06Rik, AI585793, MAPK/ERK kinase kinase 2, MEK kinase 2, MEKK 2, ...
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High impact information on Map3k2

  • Live cell fluorescence imaging of T cell MEKK2: redistribution and activation in response to antigen stimulation of the T cell receptor [1].
  • However, the identification of MEK5alpha mutants with selective binding defect demonstrates that the MEK5/ERK5 interaction does not rely on the binding of MEK5alpha to MEKK2 via their respective PB1 domains [2].
  • Mip1, an MEKK2-interacting protein, controls MEKK2 dimerization and activation [3].
  • Furthermore, TCR-mediated c-Jun N-terminal kinase activation was not blocked but moderately enhanced in Mekk2(-/-) T cells [4].
  • In conclusion, we found that MEKK2 may be required for controlling the strength of TCR/CD3 signaling [4].

Biological context of Map3k2


Anatomical context of Map3k2


Associations of Map3k2 with chemical compounds

  • Significantly, the JNK activation induced by anti-CD3 and anti-CD28 antibodies, but not by 12-O-tetradecanoylphorbol-13-acetate and Ca(2+) ionophore A23187, was inhibited by dominant negative MEKK2 mutants [5].

Regulatory relationships of Map3k2


Other interactions of Map3k2

  • However, Mekk2(-/-) T-cell proliferation was augmented in response to anti-CD3 monoclonal antibody (MAb) stimulation, and these T cells produced more interleukin 2 and gamma interferon than did the wild-type T cells, suggesting that MEKK2 may be involved in controlling the strength of T-cell receptor (TCR) signaling [4].
  • Importantly, disrupted expression of MEKK2, a related MAPK kinase kinase, had no effect on uPA activity [9].
  • The purpose of this study was to define the specific role of MEKK2, an MKKK, in MAPK regulation and cell function [7].

Analytical, diagnostic and therapeutic context of Map3k2


  1. Live cell fluorescence imaging of T cell MEKK2: redistribution and activation in response to antigen stimulation of the T cell receptor. Schaefer, B.C., Ware, M.F., Marrack, P., Fanger, G.R., Kappler, J.W., Johnson, G.L., Monks, C.R. Immunity (1999) [Pubmed]
  2. A novel mitogen-activated protein kinase docking site in the N terminus of MEK5alpha organizes the components of the extracellular signal-regulated kinase 5 signaling pathway. Seyfried, J., Wang, X., Kharebava, G., Tournier, C. Mol. Cell. Biol. (2005) [Pubmed]
  3. Mip1, an MEKK2-interacting protein, controls MEKK2 dimerization and activation. Cheng, J., Zhang, D., Kim, K., Zhao, Y., Zhao, Y., Su, B. Mol. Cell. Biol. (2005) [Pubmed]
  4. Disruption of Mekk2 in mice reveals an unexpected role for MEKK2 in modulating T-cell receptor signal transduction. Guo, Z., Clydesdale, G., Cheng, J., Kim, K., Gan, L., McConkey, D.J., Ullrich, S.E., Zhuang, Y., Su, B. Mol. Cell. Biol. (2002) [Pubmed]
  5. MEKK2 is required for T-cell receptor signals in JNK activation and interleukin-2 gene expression. Su, B., Cheng, J., Yang, J., Guo, Z. J. Biol. Chem. (2001) [Pubmed]
  6. MEF2C regulates c-Jun but not TNF-alpha gene expression in stimulated mast cells. Wei, X., Sun, W., Fan, R., Hahn, J., Joetham, A., Li, G., Webb, S., Garrington, T., Dakhama, A., Lucas, J., Johnson, G.L., Gelfand, E.W. Eur. J. Immunol. (2003) [Pubmed]
  7. MEKK2 regulates the coordinate activation of ERK5 and JNK in response to FGF-2 in fibroblasts. Kesavan, K., Lobel-Rice, K., Sun, W., Lapadat, R., Webb, S., Johnson, G.L., Garrington, T.P. J. Cell. Physiol. (2004) [Pubmed]
  8. Protein kinase C alpha, betaI, and betaII isozymes regulate cytokine production in mast cells through MEKK2/ERK5-dependent and -independent pathways. Li, G., Lucas, J.J., Gelfand, E.W. Cell. Immunol. (2005) [Pubmed]
  9. MEKK1 is required for inducible urokinase-type plasminogen activator expression. Witowsky, J., Abell, A., Johnson, N.L., Johnson, G.L., Cuevas, B.D. J. Biol. Chem. (2003) [Pubmed]
  10. PB1 domains of MEKK2 and MEKK3 interact with the MEK5 PB1 domain for activation of the ERK5 pathway. Nakamura, K., Johnson, G.L. J. Biol. Chem. (2003) [Pubmed]
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