Abstract
The RUNX1 gene, which is essential for normal hematopoiesis, is frequently rearranged by the t(8;21) chromosomal translocation in acute myeloid leukemia. The resulting RUNX1-ETO fusion protein contributes to leukemic progression by directing aberrant association of transcriptional cofactors and epigenetic modifiers to RUNX1 target genes. For example, the GM-CSF gene is activated by RUNX1, but is repressed by RUNX1-ETO. Here we show that RUNX1 normally cooperates with the histone acetyltransferase, CBP, to regulate GM-CSF expression at two levels. Firstly, it directs the establishment of a competent chromatin environment at the GM-CSF promoter prior to gene activation. It then participates in the transcriptional activation of the promoter in response to immune stimuli. In contrast, RUNX1-ETO, which cannot associate with CBP, is unable to transactivate the GM-CSF promoter and is associated with the generation of a repressive chromatin environment at the promoter.
Original language | English |
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Pages (from-to) | 1203-13 |
Number of pages | 11 |
Journal | Leukemia Research |
Volume | 34 |
Issue number | 9 |
DOIs | |
Publication status | Published - Sept 2010 |
Bibliographical note
Copyright 2010 Elsevier Ltd. All rights reserved.Keywords
- Base Sequence
- Cell Line
- Chromatin Immunoprecipitation
- Core Binding Factor Alpha 2 Subunit
- DNA Primers
- Epigenesis, Genetic
- Granulocyte-Macrophage Colony-Stimulating Factor
- Humans
- Promoter Regions, Genetic
- RNA, Small Interfering
- Transcription, Genetic