Leukemia Research
Volume 26, Issue 3 , Pages 221-228, March 2002

Runx1/AML1 in leukemia: disrupted association with diverse protein partners

  • Chava Perry

      Affiliations

    • Department of Biological Chemistry, The Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel
    • Department of Hematology, Sackler Faculty of Medicine, Tel Aviv Sourasky Medical Center, Tel-Aviv University, Tel Aviv 64239, Israel
    • ,
  • Amiram Eldor

      Affiliations

    • Department of Hematology, Sackler Faculty of Medicine, Tel Aviv Sourasky Medical Center, Tel-Aviv University, Tel Aviv 64239, Israel
    • ,
  • Hermona Soreq

      Affiliations

    • Department of Biological Chemistry, The Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem 91904, Israel
    • Corresponding Author InformationCorresponding author. Tel.: +972-2-658-5109; fax: +972-2-652-0258

Received 11 July 2001; accepted 11 July 2001.

Abstract 

Runx1/AML1, a chromosome 21q22 hematopoietic regulator, is frequently translocated in leukemia. Its protein product, a relatively weak transcriptional activator, becomes an effective transcriptional enhancer or repressor, when co-operating with transcriptional co-activators or co-repressors. Runx1/AML1 association with its partners is disrupted in leukemia. For example, Runx1/AML1 mutations and translocations (e.g. t(8;21), t(12;21) and t(3;21)) impair binding of Runx1/AML1–CBFβ complexes to Runt motifs in myelopoietically active promoters, preventing normal hematopoiesis. However, Runx1/AML1-associated translocations are not leukemogenic in animal models, suggesting the involvement of yet unidentified regulatory proteins. New candidates are cholinesterases, inhibition of which increases leukemic risk in a manner potentially associated with Runx1/AML1.

Keywords:  AML1/ETO, Cholinesterase, Chromosomal translocation, Hematopoietic malignancies, Runx1/AML1, Transcription

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PII: S0145-2126(01)00128-X

Leukemia Research
Volume 26, Issue 3 , Pages 221-228, March 2002

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