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Gene Review

Runx1  -  runt-related transcription factor 1

Rattus norvegicus

Synonyms: Acute myeloid leukemia 1 protein, Aml1, CBF-alpha-2, Cbfa2, Core-binding factor subunit alpha-2, ...
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Disease relevance of Runx1


High impact information on Runx1

  • Smad-Runx complexes are associated in situ with the nuclear matrix, and this association requires the intranuclear targeting signal of Runx factors [4].
  • Thus, Runx-mediated intranuclear targeting of Smads is critical for the integration of two distinct pathways essential for fetal development [4].
  • Development of resistance to cytarabine (AraC) is a major problem in the treatment of patients with acute myeloid leukemia (AML) [5].
  • Deletion of exons 3 to 6 was also identified in 6 of 12 PHA T cells generated from the patients with resistant AML [6].
  • In this study, we utilized retroviral transfer of cDNA libraries in order to identify oncogenes that are expressed in acute myeloid leukemia (AML) [7].

Biological context of Runx1

  • These results are consistent with the idea that AML1 may have a role in regulating gene expression in skeletal muscle [8].
  • Exposure to prostaglandin E(2) increased Runx-dependent gene transactivation independently of Runx2 binding to DNA [9].
  • C/EBPdelta gene promoter activity was reduced by mutating the Runx binding sequence or by co-transfecting with Runx2 antisense expression plasmid, and was enhanced by overexpression of Runx-2 [9].
  • FAST and Runx (CBFa) transcription factors, which are expressed during specific phases of embryogenesis and tissue patterning, bind directly to Smad proteins and integrate effects induced by various TGF-beta gene family members [10].
  • These data suggest that MLL duplications are not implicated in the malignant transformation in AML, or alternatively, that only a few cells will acquire additional oncogenic mutations necessary to establish the malignant phenotype of AML [11].

Anatomical context of Runx1

  • AML1 is expressed in skeletal muscle and is regulated by innervation [8].
  • We transfected C2 muscle cells with an expression vector encoding AML1, tagged with an epitope from hemagglutinin, and we show that AML1 is a nuclear protein in muscle [8].
  • Finally, estrogen increases gene transcription by the transforming growth factor-beta type I receptor gene promoter, which contains several Runx binding sequences, and enhances Smad dependent gene expression by transforming growth factor-beta in osteoblasts [12].
  • It was found on the cell surface of acute myeloid leukemia (AML) blasts and cell lines derived from nonhematopoietic tissues [13].
  • In both the thin-agar-layer system, which uses a feeder layer of fetal fibroblasts, and the Robinson culture system, human AML marrow failed to produce colonies [1].

Associations of Runx1 with chemical compounds


Other interactions of Runx1


Analytical, diagnostic and therapeutic context of Runx1

  • Four AML1 transcripts are expressed in denervated muscle, and the abundance of each transcript increases after denervation [8].
  • Further studies with this animal model of AML, in which resistance to CY is mediated by elevated ALDH activity, may elucidate mechanisms for effective elimination of drug-resistant leukemic cells ex vivo and in vivo [14].
  • We have detected expression of DeltaTrkA in the original AML sample by reverse transcriptase PCR and by Western blot analysis [7].
  • To study prognostic factors in infant acute myeloid leukemia (AML), we analyzed 44 children treated on Childrens Cancer Group protocols for MLL gene rearrangement by Southern blot, cytogenetic 11q23 abnormalities, and reactivity with monoclonal antibody 7 [20].
  • We conclude that CFU-Leuk and CFU-GM assays are useful screening techniques to develop and evaluate strategies for ex vivo purging with chemotherapeutic agents in this preclinical model of autologous marrow transplantation for AML [21].


  1. In vitro colony formation of transplantable rat leukemias in comparison with human acute myeloid leukemia. van Bekkum, D.W., van Oosterom, P., Dicke, K.A. Cancer Res. (1976) [Pubmed]
  2. Broad distribution of the multidrug resistance-related vault lung resistance protein in normal human tissues and tumors. Izquierdo, M.A., Scheffer, G.L., Flens, M.J., Giaccone, G., Broxterman, H.J., Meijer, C.J., van der Valk, P., Scheper, R.J. Am. J. Pathol. (1996) [Pubmed]
  3. Nitrous oxide reduces growth of experimental rat leukemia. Kroes, A.C., Lindemans, J., Hagenbeek, A., Abels, J. Leuk. Res. (1984) [Pubmed]
  4. Integration of Runx and Smad regulatory signals at transcriptionally active subnuclear sites. Zaidi, S.K., Sullivan, A.J., van Wijnen, A.J., Stein, J.L., Stein, G.S., Lian, J.B. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  5. Functional role of alternatively spliced deoxycytidine kinase in sensitivity to cytarabine of acute myeloid leukemic cells. Veuger, M.J., Heemskerk, M.H., Honders, M.W., Willemze, R., Barge, R.M. Blood (2002) [Pubmed]
  6. High incidence of alternatively spliced forms of deoxycytidine kinase in patients with resistant acute myeloid leukemia. Veuger, M.J., Honders, M.W., Landegent, J.E., Willemze, R., Barge, R.M. Blood (2000) [Pubmed]
  7. Identification and characterization of an activating TrkA deletion mutation in acute myeloid leukemia. Reuther, G.W., Lambert, Q.T., Caligiuri, M.A., Der, C.J. Mol. Cell. Biol. (2000) [Pubmed]
  8. AML1 is expressed in skeletal muscle and is regulated by innervation. Zhu, X., Yeadon, J.E., Burden, S.J. Mol. Cell. Biol. (1994) [Pubmed]
  9. Runt domain factor (Runx)-dependent effects on CCAAT/ enhancer-binding protein delta expression and activity in osteoblasts. McCarthy, T.L., Ji, C., Chen, Y., Kim, K.K., Imagawa, M., Ito, Y., Centrella, M. J. Biol. Chem. (2000) [Pubmed]
  10. Control and counter-control of TGF-beta activity through FAST and Runx (CBFa) transcriptional elements in osteoblasts. Ji, C., Eickelberg, O., McCarthy, T.L., Centrella, M. Endocrinology (2001) [Pubmed]
  11. Partial tandem duplications of the MLL gene are detectable in peripheral blood and bone marrow of nearly all healthy donors. Schnittger, S., Wörmann, B., Hiddemann, W., Griesinger, F. Blood (1998) [Pubmed]
  12. Runx2 integrates estrogen activity in osteoblasts. McCarthy, T.L., Chang, W.Z., Liu, Y., Centrella, M. J. Biol. Chem. (2003) [Pubmed]
  13. The human homologue of rat NG2, a chondroitin sulfate proteoglycan, is not expressed on the cell surface of normal hematopoietic cells but is expressed by acute myeloid leukemia blasts from poor-prognosis patients with abnormalities of chromosome band 11q23. Smith, F.O., Rauch, C., Williams, D.E., March, C.J., Arthur, D., Hilden, J., Lampkin, B.C., Buckley, J.D., Buckley, C.V., Woods, W.G., Dinndorf, P.A., Sorensen, P., Kersey, J., Hammond, D., Bernstein, I.D. Blood (1996) [Pubmed]
  14. Development and characterization of a cyclophosphamide-resistant subline of acute myeloid leukemia in the Lewis x Brown Norway hybrid rat. Koelling, T.M., Yeager, A.M., Hilton, J., Haynie, D.T., Wiley, J.M. Blood (1990) [Pubmed]
  15. Differences in the pharmacokinetics of daunomycin in normal and leukemic rats. Nooter, K., Sonneveld, P., Martens, A. Cancer Res. (1985) [Pubmed]
  16. Role of deoxycytidine kinase in an in vitro model for AraC- and DAC-resistance: substrate-enzyme interactions with deoxycytidine, 1-beta-D-arabinofuranosylcytosine and 5-aza-2'-deoxycytidine. Stegmann, A.P., Honders, M.W., Kester, M.G., Landegent, J.E., Willemze, R. Leukemia (1993) [Pubmed]
  17. Reduced CpG methylation is associated with transcriptional activation of the bone-specific rat osteocalcin gene in osteoblasts. Villagra, A., Gutiérrez, J., Paredes, R., Sierra, J., Puchi, M., Imschenetzky, M., Wijnen Av, A., Lian, J., Stein, G., Stein, J., Montecino, M. J. Cell. Biochem. (2002) [Pubmed]
  18. In vitro-induced resistance to the deoxycytidine analogues cytarabine (AraC) and 5-aza-2'-deoxycytidine (DAC) in a rat model for acute myeloid leukemia is mediated by mutations in the deoxycytidine kinase (dck) gene. Stegmann, A.P., Honders, M.W., Hagemeijer, A., Hoebee, B., Willemze, R., Landegent, J.E. Ann. Hematol. (1995) [Pubmed]
  19. Diphtheria toxin-murine granulocyte-macrophage colony-stimulating factor-induced hepatotoxicity is mediated by Kupffer cells. Westcott, M.M., Abi-Habib, R.J., Cohen, K.A., Willingham, M.C., Liu, S., Bugge, T.H., Leppla, S.H., Frankel, A.E. Mol. Cancer Ther. (2004) [Pubmed]
  20. MLL gene rearrangement, cytogenetic 11q23 abnormalities, and expression of the NG2 molecule in infant acute myeloid leukemia. Hilden, J.M., Smith, F.O., Frestedt, J.L., McGlennen, R., Howells, W.B., Sorensen, P.H., Arthur, D.C., Woods, W.G., Buckley, J., Bernstein, I.D., Kersey, J.H. Blood (1997) [Pubmed]
  21. Predictive value of colony-forming unit assays for engraftment and leukemia-free survival after transplantation of chemopurged syngeneic bone marrow in rats. Wiley, J.M., Yeager, A.M. Exp. Hematol. (1991) [Pubmed]
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