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

Chava Perry, Amiram Eldor, Hermona Soreq*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

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.

Original languageEnglish
Pages (from-to)221-228
Number of pages8
JournalLeukemia Research
Volume26
Issue number3
DOIs
StatePublished - 2002

Keywords

  • AML1/ETO
  • Cholinesterase
  • Chromosomal translocation
  • Hematopoietic malignancies
  • Runx1/AML1
  • Transcription

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