Epigenetic consequences of AML1-ETO action at the human c-FMS locus

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Epigenetic consequences of AML1-ETO action at the human c-FMS locus. / Follows, GA; Tagoh, H; Lefevre, P; Hodge, D; Morgan, GJ; Bonifer, Constanze.

In: The EMBO journal, Vol. 22, No. 11, 02.06.2003, p. 2798-809.

Research output: Contribution to journalArticle

Harvard

Follows, GA, Tagoh, H, Lefevre, P, Hodge, D, Morgan, GJ & Bonifer, C 2003, 'Epigenetic consequences of AML1-ETO action at the human c-FMS locus', The EMBO journal, vol. 22, no. 11, pp. 2798-809. https://doi.org/10.1093/emboj/cdg250

APA

Follows, GA., Tagoh, H., Lefevre, P., Hodge, D., Morgan, GJ., & Bonifer, C. (2003). Epigenetic consequences of AML1-ETO action at the human c-FMS locus. The EMBO journal, 22(11), 2798-809. https://doi.org/10.1093/emboj/cdg250

Vancouver

Author

Follows, GA ; Tagoh, H ; Lefevre, P ; Hodge, D ; Morgan, GJ ; Bonifer, Constanze. / Epigenetic consequences of AML1-ETO action at the human c-FMS locus. In: The EMBO journal. 2003 ; Vol. 22, No. 11. pp. 2798-809.

Bibtex

@article{c172fc670c29415fb7fc7c85620540d0,
title = "Epigenetic consequences of AML1-ETO action at the human c-FMS locus",
abstract = "Although many leukaemia-associated nuclear oncogenes are well characterized, little is known about the molecular details of how they alter gene expression. Here we examined transcription factor complexes and chromatin structure of the human c-FMS gene in normal and leukaemic cells. We demonstrate by in vivo footprinting and chromatin immunoprecipitation assays that this gene is bound by the transcription factor AML1 (RUNX1). In t(8;21) leukaemic cells expressing the aberrant fusion protein AML1-ETO, we demonstrate that this protein is part of a transcription factor complex binding to extended sequences of the c-FMS intronic regulatory region rather than the promoter. The AML1-ETO complex does not disrupt binding of other transcription factors, indicating that c-FMS is not irreversibly epigenetically silenced. However, AML1-ETO binding correlates with changes in the histone modification pattern and increased association of histone deacetylases. Our experiments provide for the first time a direct insight into the chromatin structure of an AML1-ETO-bound target gene.",
author = "GA Follows and H Tagoh and P Lefevre and D Hodge and GJ Morgan and Constanze Bonifer",
year = "2003",
month = jun,
day = "2",
doi = "10.1093/emboj/cdg250",
language = "English",
volume = "22",
pages = "2798--809",
journal = "The EMBO journal",
issn = "0261-4189",
publisher = "EMBO Press",
number = "11",

}

RIS

TY - JOUR

T1 - Epigenetic consequences of AML1-ETO action at the human c-FMS locus

AU - Follows, GA

AU - Tagoh, H

AU - Lefevre, P

AU - Hodge, D

AU - Morgan, GJ

AU - Bonifer, Constanze

PY - 2003/6/2

Y1 - 2003/6/2

N2 - Although many leukaemia-associated nuclear oncogenes are well characterized, little is known about the molecular details of how they alter gene expression. Here we examined transcription factor complexes and chromatin structure of the human c-FMS gene in normal and leukaemic cells. We demonstrate by in vivo footprinting and chromatin immunoprecipitation assays that this gene is bound by the transcription factor AML1 (RUNX1). In t(8;21) leukaemic cells expressing the aberrant fusion protein AML1-ETO, we demonstrate that this protein is part of a transcription factor complex binding to extended sequences of the c-FMS intronic regulatory region rather than the promoter. The AML1-ETO complex does not disrupt binding of other transcription factors, indicating that c-FMS is not irreversibly epigenetically silenced. However, AML1-ETO binding correlates with changes in the histone modification pattern and increased association of histone deacetylases. Our experiments provide for the first time a direct insight into the chromatin structure of an AML1-ETO-bound target gene.

AB - Although many leukaemia-associated nuclear oncogenes are well characterized, little is known about the molecular details of how they alter gene expression. Here we examined transcription factor complexes and chromatin structure of the human c-FMS gene in normal and leukaemic cells. We demonstrate by in vivo footprinting and chromatin immunoprecipitation assays that this gene is bound by the transcription factor AML1 (RUNX1). In t(8;21) leukaemic cells expressing the aberrant fusion protein AML1-ETO, we demonstrate that this protein is part of a transcription factor complex binding to extended sequences of the c-FMS intronic regulatory region rather than the promoter. The AML1-ETO complex does not disrupt binding of other transcription factors, indicating that c-FMS is not irreversibly epigenetically silenced. However, AML1-ETO binding correlates with changes in the histone modification pattern and increased association of histone deacetylases. Our experiments provide for the first time a direct insight into the chromatin structure of an AML1-ETO-bound target gene.

U2 - 10.1093/emboj/cdg250

DO - 10.1093/emboj/cdg250

M3 - Article

C2 - 12773394

VL - 22

SP - 2798

EP - 2809

JO - The EMBO journal

JF - The EMBO journal

SN - 0261-4189

IS - 11

ER -