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Gene Review

Tak1  -  TGF-beta activated kinase 1

Drosophila melanogaster

Synonyms: CG1388, CG18492, D-TAK, D-tak, D10, ...
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High impact information on Tak1

  • Relish activation is linked to proteasomal degradation of TAK1, the upstream MAP kinase kinase kinase required for JNK activation [1].
  • Moreover, depletion of either TAK1 or NLK inhibits endogenous serine phosphorylation of STAT3 [2].
  • Depletion of TAK1, NLK, or STAT3 blocks TGF-beta-mediated mesoderm induction [2].
  • Mutations in the Drosophila dTAK1 gene reveal a conserved function for MAPKKKs in the control of rel/NF-kappaB-dependent innate immune responses [3].
  • TAK1 function has largely been studied in cultured cells, and its in vivo function is not fully understood [3].

Biological context of Tak1


Anatomical context of Tak1

  • Furthermore, overexpression of dominant negative (DN) or wild-type forms of dTAK in wing and eye imaginal discs, respectively, results in defects in thorax closure and ommatidial planar polarity, two well described phenotypes associated with JNK signaling activity [4].
  • TAK1 function has been extensively studied in cultured cells, but its in vivo function is not fully understood [5].
  • The RS fibroblasts with the heterochromatin abnormality were consistently more sensitive (based on D10 values) to mitomycin C treatment than were any of the other cell strains tested, including RS(-) cells [8].

Associations of Tak1 with chemical compounds


Physical interactions of Tak1

  • Activation of the DmIKK complex requires the MAP3K dTAK1, but the mechanism of dTAK1 activation is not understood [10].

Regulatory relationships of Tak1

  • In this report, we demonstrate that Drosophila TAK1 functions as both the Drosophila IkappaB kinase-activating kinase and the JNK kinase-activating kinase [11].

Other interactions of Tak1

  • Genetic and biochemical analyses also indicate that the c-Jun amino-terminal kinase (JNK) signaling pathway is specifically activated by TAK1 signaling [5].
  • However, we demonstrate that Relish activation is intact in dTAK1 mutant animals, and that the immune response in these mutant animals was rescued by overexpression of a downstream JNKK [6].
  • Here we demonstrate that the Drosophila homologs of Ubc13 and UEV1a are similarly required for the activation of dTAK1 and the DmIKK complex [10].


  1. Targeting of TAK1 by the NF-kappa B protein Relish regulates the JNK-mediated immune response in Drosophila. Park, J.M., Brady, H., Ruocco, M.G., Sun, H., Williams, D., Lee, S.J., Kato, T., Richards, N., Chan, K., Mercurio, F., Karin, M., Wasserman, S.A. Genes Dev. (2004) [Pubmed]
  2. Role of the TAK1-NLK-STAT3 pathway in TGF-beta-mediated mesoderm induction. Ohkawara, B., Shirakabe, K., Hyodo-Miura, J., Matsuo, R., Ueno, N., Matsumoto, K., Shibuya, H. Genes Dev. (2004) [Pubmed]
  3. Mutations in the Drosophila dTAK1 gene reveal a conserved function for MAPKKKs in the control of rel/NF-kappaB-dependent innate immune responses. Vidal, S., Khush, R.S., Leulier, F., Tzou, P., Nakamura, M., Lemaitre, B. Genes Dev. (2001) [Pubmed]
  4. The role of the Drosophila TAK homologue dTAK during development. Mihaly, J., Kockel, L., Gaengel, K., Weber, U., Bohmann, D., Mlodzik, M. Mech. Dev. (2001) [Pubmed]
  5. TAK1 participates in c-Jun N-terminal kinase signaling during Drosophila development. Takatsu, Y., Nakamura, M., Stapleton, M., Danos, M.C., Matsumoto, K., O'Connor, M.B., Shibuya, H., Ueno, N. Mol. Cell. Biol. (2000) [Pubmed]
  6. Cooperative control of Drosophila immune responses by the JNK and NF-kappaB signaling pathways. Delaney, J.R., Stöven, S., Uvell, H., Anderson, K.V., Engström, Y., Mlodzik, M. EMBO J. (2006) [Pubmed]
  7. A genetic screen targeting the tumor necrosis factor/Eiger signaling pathway: identification of Drosophila TAB2 as a functionally conserved component. Geuking, P., Narasimamurthy, R., Basler, K. Genetics (2005) [Pubmed]
  8. Hypersensitivity to mitomycin C cell-killing in Roberts syndrome fibroblasts with, but not without, the heterochromatin abnormality. Burns, M.A., Tomkins, D.J. Mutat. Res. (1989) [Pubmed]
  9. Stimulus-specific requirements for MAP3 kinases in activating the JNK pathway. Chen, W., White, M.A., Cobb, M.H. J. Biol. Chem. (2002) [Pubmed]
  10. The role of ubiquitination in Drosophila innate immunity. Zhou, R., Silverman, N., Hong, M., Liao, D.S., Chung, Y., Chen, Z.J., Maniatis, T. J. Biol. Chem. (2005) [Pubmed]
  11. Immune activation of NF-kappaB and JNK requires Drosophila TAK1. Silverman, N., Zhou, R., Erlich, R.L., Hunter, M., Bernstein, E., Schneider, D., Maniatis, T. J. Biol. Chem. (2003) [Pubmed]
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