CBFB–MYH11/RUNX1 together with a compendium of hematopoietic regulators, chromatin modifiers and basal transcription factors occupies self-renewal genes in inv(16) acute myeloid leukemia

@article{Mandoli2014CBFBMYH11RUNX1TW,
  title={CBFB–MYH11/RUNX1 together with a compendium of hematopoietic regulators, chromatin modifiers and basal transcription factors occupies self-renewal genes in inv(16) acute myeloid leukemia},
  author={A Soler Mandoli and Abhishek A. Singh and Pascal W. T. C. Jansen and Albertus T. J. Wierenga and Homayoun Riahi and Gianluigi Franci and Koen H. M. Prange and Sadia Saeed and Edo Vellenga and M{\'o}nica Vermeulen and Hendrik G. Stunnenberg and Joost H. A. Martens},
  journal={Leukemia},
  year={2014},
  volume={28},
  pages={770-778}
}
Different mechanisms for CBFβ–MYH11 function in acute myeloid leukemia with inv(16) have been proposed such as tethering of RUNX1 outside the nucleus, interference with transcription factor complex assembly and recruitment of histone deacetylases, all resulting in transcriptional repression of RUNX1 target genes. Here, through genome-wide CBFβ–MYH11-binding site analysis and quantitative interaction proteomics, we found that CBFβ–MYH11 localizes to RUNX1 occupied promoters, where it interacts… CONTINUE READING

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Different mechanisms for CBFβ–MYH11 function in acute myeloid leukemia with inv(16 ) have been proposed such as tethering of RUNX1 outside the nucleus , interference with transcription factor complex assembly and recruitment of histone deacetylases , all resulting in transcriptional repression of RUNX1 target genes .
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