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Gene Review

Mecom  -  MDS1 and EVI1 complex locus

Mus musculus

Synonyms: D630039M04Rik, Evi-1, Evi1, Jbo, MDS1 and EVI1 complex locus protein MDS1, ...
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Disease relevance of Evi1


High impact information on Evi1


Biological context of Evi1

  • Taken together, our results present the first evidence of Evi1 disturbing normal erythropoiesis in vivo and provides evidence for cooperative potential of Evi1 in tumor progression [8].
  • The full-length Evi1 transcript encodes a putative transcription factor, containing ten zinc finger motifs found within two domains of the protein [9].
  • The Evi1 proto-oncogene is required at midgestation for neural, heart, and paraxial mesenchyme development [9].
  • These data suggest that Evi1 has important roles in general cell proliferation, vascularization, and cell-specific developmental signaling, at midgestation [9].
  • To determine the biological function of the Evi1 proto-oncogene, the full-length, but not an alternately spliced, transcript was disrupted using targeted mutagenesis in embryonic stem cells [9].

Anatomical context of Evi1


Associations of Evi1 with chemical compounds

  • After retinoic acid (RA) treatment with aggregation, expression of Evi1 was detected during neural differentiation in P19 cells [4].
  • However, Evi1 was not expressed in P19 cells during mesodermal differentiation after DMSO treatment with aggregation [4].
  • In the studies presented here we also show that Evi-1 can repress GATA-1-dependent transactivation in transient chloramphenicol acetyltransferase assays [14].
  • Both GAL4DBD/Evi-1 fusion and non-fusion proteins have been used to map the repressor activity to a proline-rich region located within amino acids 514-724 between the ZF1 and ZF2 domains [15].

Regulatory relationships of Evi1


Other interactions of Evi1


Analytical, diagnostic and therapeutic context of Evi1

  • These results correlated with whole-mount in situ hybridization analyses of embryos which showed expression of the Evi1 proto-oncogene in embryonic mesoderm and neural crest-derived cells associated with the peripheral nervous system [9].
  • The possible basis for the unique expression of the Evi-1 gene by HEC-1 cells could not be determined by karyotype or Southern blot analysis [5].
  • By sequence analysis, we found that one Evi-1 cDNA (E29) had an internal deletion of 972 nucleotides when compared to the full-length sequence previously published by Morishita et al [19].
  • To evaluate the sequence specificity of Evi-1 binding and potentially identify genomic targets, whole-genome PCR was utilized to isolate multiple Sau3A fragments which specifically bind to the amino-terminal zinc finger domain [20].


  1. Phenotyping of Evi1, Evi11/Cb2, and Evi12 transformed leukemias isolated from a novel panel of cas-Br-M murine leukemia virus-infected mice. Joosten, M., Valk, P.J., Vankan, Y., de Both, N., Löwenberg, B., Delwel, R. Virology (2000) [Pubmed]
  2. Chromosomal location of Evi-1, a common site of ecotropic viral integration in AKXD murine myeloid tumors. Mucenski, M.L., Taylor, B.A., Copeland, N.G., Jenkins, N.A. Oncogene Res. (1988) [Pubmed]
  3. Retroviral activation of a novel gene encoding a zinc finger protein in IL-3-dependent myeloid leukemia cell lines. Morishita, K., Parker, D.S., Mucenski, M.L., Jenkins, N.A., Copeland, N.G., Ihle, J.N. Cell (1988) [Pubmed]
  4. Ecotropic viral integration site-1 is activated during, and is sufficient for, neuroectodermal P19 cell differentiation. Kazama, H., Kodera, T., Shimizu, S., Mizoguchi, H., Morishita, K. Cell Growth Differ. (1999) [Pubmed]
  5. Unique expression of the human Evi-1 gene in an endometrial carcinoma cell line: sequence of cDNAs and structure of alternatively spliced transcripts. Morishita, K., Parganas, E., Douglass, E.C., Ihle, J.N. Oncogene (1990) [Pubmed]
  6. Oncogenic transcription factor Evi1 regulates hematopoietic stem cell proliferation through GATA-2 expression. Yuasa, H., Oike, Y., Iwama, A., Nishikata, I., Sugiyama, D., Perkins, A., Mucenski, M.L., Suda, T., Morishita, K. EMBO J. (2005) [Pubmed]
  7. Retroviral integration in murine myeloid tumors to identify Evi-1, a novel locus encoding a zinc-finger protein. Copeland, N.G., Jenkins, N.A. Adv. Cancer Res. (1990) [Pubmed]
  8. Erythroid defects and increased retrovirally-induced tumor formation in Evi1 transgenic mice. Louz, D., van den Broek, M., Verbakel, S., Vankan, Y., van Lom, K., Joosten, M., Meijer, D., Löwenberg, B., Delwel, R. Leukemia (2000) [Pubmed]
  9. The Evi1 proto-oncogene is required at midgestation for neural, heart, and paraxial mesenchyme development. Hoyt, P.R., Bartholomew, C., Davis, A.J., Yutzey, K., Gamer, L.W., Potter, S.S., Ihle, J.N., Mucenski, M.L. Mech. Dev. (1997) [Pubmed]
  10. Evi-1 raises AP-1 activity and stimulates c-fos promoter transactivation with dependence on the second zinc finger domain. Tanaka, T., Nishida, J., Mitani, K., Ogawa, S., Yazaki, Y., Hirai, H. J. Biol. Chem. (1994) [Pubmed]
  11. Identification of a common ecotropic viral integration site, Evi-1, in the DNA of AKXD murine myeloid tumors. Mucenski, M.L., Taylor, B.A., Ihle, J.N., Hartley, J.W., Morse, H.C., Jenkins, N.A., Copeland, N.G. Mol. Cell. Biol. (1988) [Pubmed]
  12. The AML1/Evi-1 fusion protein in the t(3;21) translocation exhibits transforming activity on Rat1 fibroblasts with dependence on the Evi-1 sequence. Kurokawa, M., Ogawa, S., Tanaka, T., Mitani, K., Yazaki, Y., Witte, O.N., Hirai, H. Oncogene (1995) [Pubmed]
  13. Evi-1 expression in leukemic patients with rearrangements of the 3q25-q28 chromosomal region. Fichelson, S., Dreyfus, F., Berger, R., Melle, J., Bastard, C., Miclea, J.M., Gisselbrecht, S. Leukemia (1992) [Pubmed]
  14. Loss of erythropoietin responsiveness in erythroid progenitors due to expression of the Evi-1 myeloid-transforming gene. Kreider, B.L., Orkin, S.H., Ihle, J.N. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  15. The Evi-1 proto-oncogene encodes a transcriptional repressor activity associated with transformation. Bartholomew, C., Kilbey, A., Clark, A.M., Walker, M. Oncogene (1997) [Pubmed]
  16. Retroviral insertions in the CB-1/Fim-3 common site of integration activate expression of the Evi-1 gene. Bartholomew, C., Morishita, K., Askew, D., Buchberg, A., Jenkins, N.A., Copeland, N.G., Ihle, J.N. Oncogene (1989) [Pubmed]
  17. Fim-1, Fim-2/c-fms, and Fim-3, three common integration sites of Friend murine leukemia virus in myeloblastic leukemias, map to mouse chromosomes 13, 18, and 3, respectively. Sola, B., Simon, D., Mattéi, M.G., Fichelson, S., Bordereaux, D., Tambourin, P.E., Guenet, J.L., Gisselbrecht, S. J. Virol. (1988) [Pubmed]
  18. Dual functions of the AML1/Evi-1 chimeric protein in the mechanism of leukemogenesis in t(3;21) leukemias. Tanaka, T., Mitani, K., Kurokawa, M., Ogawa, S., Tanaka, K., Nishida, J., Yazaki, Y., Shibata, Y., Hirai, H. Mol. Cell. Biol. (1995) [Pubmed]
  19. Alternative splicing of the Evi-1 zinc finger gene generates mRNAs which differ by the number of zinc finger motifs. Bordereaux, D., Fichelson, S., Tambourin, P., Gisselbrecht, S. Oncogene (1990) [Pubmed]
  20. The Evi-1 zinc finger myeloid transforming protein binds to genomic fragments containing (GATA)n sequences. Matsugi, T., Kreider, B.L., Delwel, R., Cleveland, J.L., Askew, D.S., Ihle, J.N. Oncogene (1995) [Pubmed]
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