ABSTRACT _RUNX1_ (_AML1)_ is a gene that is frequently disrupted by chromosomal translocations in acute leukemia. Like its _Drosophila_ homolog Runt, RUNX1 both activates and represses

transcription. Both Runt and RUNX1 are required for gene silencing during development and a central domain of RUNX1, termed repression domain 2 (RD2), was defined as being required for

transcriptional repression and for the silencing of _CD4_ during T-cell maturation in thymic organ cultures. Although transcriptional co-repressors are known to contact other repression

domains in RUNX1, the factors that bind to RD2 had not been defined. Therefore, we tested whether RD2 contacts histone-modifying enzymes that may mediate both repression and gene silencing.

transcriptional repression. The association between RUNX1, histone deacetylases and SUV39H1 provides a molecular mechanism for repression and possibly gene silencing mediated by RUNX1.

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(1996). _Mol Cell Biol_ 16: 1231–1240. Download references ACKNOWLEDGEMENTS We thank members of the Hiebert lab for critical evaluation of the manuscript. We thank the Vanderbilt-Ingram

Cancer Center and the VICC DNA sequencing core for support. This work was supported by NIH/NCI grants RO1-CA64140, RO1-CA77274, and RO1-87549 (SWH), RO1-HL49118 (SJB), a Merit Review Award

from the Department of Veterans Affairs (SJB), and a Center grant from the National Cancer Institute (CA68485). BJI was a fellow of the Leukemia and Lymphoma Society of America. AUTHOR

INFORMATION Author notes * E Reed-Inderbitzin Present address: University of Oregon Health Sciences Center, Beaverton, OR, USA * B Lutterbach Present address: Merck Inc., West Point, PA, USA

* K L Durst-Goodwin Present address: Indiana University School of Medicine, Indianapolis, IN, USA * B J Irvin Present address: The Blood Center of Wisconsin, Milwaukee, WI, USA * E

Reed-Inderbitzin, I Moreno-Miralles and S K Vanden-Eynden: These authors contributed equally to this work. AUTHORS AND AFFILIATIONS * Department of Biochemistry, Vanderbilt University School

of Medicine, Nashville, TN, USA E Reed-Inderbitzin, I Moreno-Miralles, S K Vanden-Eynden, B Lutterbach, K L Durst-Goodwin, K S Luce, B J Irvin & S W Hiebert * Department of Medicine,

Vanderbilt University School of Medicine, Nashville, TN, USA J Xie & S J Brandt * Stanford University Medical School, Palo Alto, CA, USA M L Cleary * Cell and Developmental Biology,

Vanderbilt University School of Medicine, Nashville, TN, USA S J Brandt * Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA S J Brandt * Vanderbilt-Ingram Cancer

Center, Vanderbilt University School of Medicine, Nashville, TN, USA S J Brandt & S W Hiebert * Tennessee Valley VA Healthcare System, Nashville, TN, USA S J Brandt Authors * E

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RUNX1 associates with histone deacetylases and SUV39H1 to repress transcription. _Oncogene_ 25, 5777–5786 (2006). https://doi.org/10.1038/sj.onc.1209591 Download citation * Received: 19

April 2005 * Revised: 21 February 2006 * Accepted: 28 February 2006 * Published: 01 May 2006 * Issue Date: 21 September 2006 * DOI: https://doi.org/10.1038/sj.onc.1209591 SHARE THIS ARTICLE

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by the Springer Nature SharedIt content-sharing initiative KEYWORDS * Suv39h1 * RUNX1 * AML1 * histone * deacetylase