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 demon...
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Autor*in:	Follows, George A. [verfasserIn] Tagoh, Hiromi [verfasserIn] Lefevre, Pascal [verfasserIn] Hodge, Donald [verfasserIn] Morgan, Gareth J. [verfasserIn] Bonifer, Constanze [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2003

Schlagwörter:	AML1–ETO c‐FMS chromatin HDAC‐1 t(8;21) leukaemia

Anmerkung:	© European Molecular Biology Organization 2003

Übergeordnetes Werk:	Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 22(2003), 11 vom: 01. Juni, Seite 2798-2809
Übergeordnetes Werk:	volume:22 ; year:2003 ; number:11 ; day:01 ; month:06 ; pages:2798-2809

Links:	Volltext

DOI / URN:	10.1093/emboj/cdg250

Katalog-ID:	SPR058009523

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520			\|a 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.
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allfields	10.1093/emboj/cdg250 doi (DE-627)SPR058009523 (SPR)cdg250-e DE-627 ger DE-627 rakwb eng Follows, George A. verfasserin aut Epigenetic consequences of AML1–ETO action at the human c‐FMS locus 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2003 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. AML1–ETO (dpeaa)DE-He213 c‐FMS (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 HDAC‐1 (dpeaa)DE-He213 t(8;21) leukaemia (dpeaa)DE-He213 Tagoh, Hiromi verfasserin aut Lefevre, Pascal verfasserin aut Hodge, Donald verfasserin aut Morgan, Gareth J. verfasserin aut Bonifer, Constanze verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 22(2003), 11 vom: 01. Juni, Seite 2798-2809 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809 https://dx.doi.org/10.1093/emboj/cdg250 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 22 2003 11 01 06 2798-2809
spelling	10.1093/emboj/cdg250 doi (DE-627)SPR058009523 (SPR)cdg250-e DE-627 ger DE-627 rakwb eng Follows, George A. verfasserin aut Epigenetic consequences of AML1–ETO action at the human c‐FMS locus 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2003 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. AML1–ETO (dpeaa)DE-He213 c‐FMS (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 HDAC‐1 (dpeaa)DE-He213 t(8;21) leukaemia (dpeaa)DE-He213 Tagoh, Hiromi verfasserin aut Lefevre, Pascal verfasserin aut Hodge, Donald verfasserin aut Morgan, Gareth J. verfasserin aut Bonifer, Constanze verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 22(2003), 11 vom: 01. Juni, Seite 2798-2809 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809 https://dx.doi.org/10.1093/emboj/cdg250 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 22 2003 11 01 06 2798-2809
allfields_unstemmed	10.1093/emboj/cdg250 doi (DE-627)SPR058009523 (SPR)cdg250-e DE-627 ger DE-627 rakwb eng Follows, George A. verfasserin aut Epigenetic consequences of AML1–ETO action at the human c‐FMS locus 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2003 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. AML1–ETO (dpeaa)DE-He213 c‐FMS (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 HDAC‐1 (dpeaa)DE-He213 t(8;21) leukaemia (dpeaa)DE-He213 Tagoh, Hiromi verfasserin aut Lefevre, Pascal verfasserin aut Hodge, Donald verfasserin aut Morgan, Gareth J. verfasserin aut Bonifer, Constanze verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 22(2003), 11 vom: 01. Juni, Seite 2798-2809 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809 https://dx.doi.org/10.1093/emboj/cdg250 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 22 2003 11 01 06 2798-2809
allfieldsGer	10.1093/emboj/cdg250 doi (DE-627)SPR058009523 (SPR)cdg250-e DE-627 ger DE-627 rakwb eng Follows, George A. verfasserin aut Epigenetic consequences of AML1–ETO action at the human c‐FMS locus 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2003 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. AML1–ETO (dpeaa)DE-He213 c‐FMS (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 HDAC‐1 (dpeaa)DE-He213 t(8;21) leukaemia (dpeaa)DE-He213 Tagoh, Hiromi verfasserin aut Lefevre, Pascal verfasserin aut Hodge, Donald verfasserin aut Morgan, Gareth J. verfasserin aut Bonifer, Constanze verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 22(2003), 11 vom: 01. Juni, Seite 2798-2809 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809 https://dx.doi.org/10.1093/emboj/cdg250 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 22 2003 11 01 06 2798-2809
allfieldsSound	10.1093/emboj/cdg250 doi (DE-627)SPR058009523 (SPR)cdg250-e DE-627 ger DE-627 rakwb eng Follows, George A. verfasserin aut Epigenetic consequences of AML1–ETO action at the human c‐FMS locus 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2003 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. AML1–ETO (dpeaa)DE-He213 c‐FMS (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 HDAC‐1 (dpeaa)DE-He213 t(8;21) leukaemia (dpeaa)DE-He213 Tagoh, Hiromi verfasserin aut Lefevre, Pascal verfasserin aut Hodge, Donald verfasserin aut Morgan, Gareth J. verfasserin aut Bonifer, Constanze verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 22(2003), 11 vom: 01. Juni, Seite 2798-2809 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809 https://dx.doi.org/10.1093/emboj/cdg250 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 22 2003 11 01 06 2798-2809
language	English
source	Enthalten in The EMBO Journal 22(2003), 11 vom: 01. Juni, Seite 2798-2809 volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809
sourceStr	Enthalten in The EMBO Journal 22(2003), 11 vom: 01. Juni, Seite 2798-2809 volume:22 year:2003 number:11 day:01 month:06 pages:2798-2809
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institution	findex.gbv.de
topic_facet	AML1–ETO c‐FMS chromatin HDAC‐1 t(8;21) leukaemia
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container_title	The EMBO Journal
authorswithroles_txt_mv	Follows, George A. @@aut@@ Tagoh, Hiromi @@aut@@ Lefevre, Pascal @@aut@@ Hodge, Donald @@aut@@ Morgan, Gareth J. @@aut@@ Bonifer, Constanze @@aut@@
publishDateDaySort_date	2003-06-01T00:00:00Z
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author	Follows, George A.
spellingShingle	Follows, George A. misc AML1–ETO misc c‐FMS misc chromatin misc HDAC‐1 misc t(8;21) leukaemia Epigenetic consequences of AML1–ETO action at the human c‐FMS locus
authorStr	Follows, George A.
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topic_title	Epigenetic consequences of AML1–ETO action at the human c‐FMS locus AML1–ETO (dpeaa)DE-He213 c‐FMS (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 HDAC‐1 (dpeaa)DE-He213 t(8;21) leukaemia (dpeaa)DE-He213
topic	misc AML1–ETO misc c‐FMS misc chromatin misc HDAC‐1 misc t(8;21) leukaemia
topic_unstemmed	misc AML1–ETO misc c‐FMS misc chromatin misc HDAC‐1 misc t(8;21) leukaemia
topic_browse	misc AML1–ETO misc c‐FMS misc chromatin misc HDAC‐1 misc t(8;21) leukaemia
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title	Epigenetic consequences of AML1–ETO action at the human c‐FMS locus
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title_full	Epigenetic consequences of AML1–ETO action at the human c‐FMS locus
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title_sort	epigenetic consequences of aml1–eto action at the human c‐fms locus
title_auth	Epigenetic consequences of AML1–ETO action at the human c‐FMS locus
abstract	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. © European Molecular Biology Organization 2003
abstractGer	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. © European Molecular Biology Organization 2003
abstract_unstemmed	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. © European Molecular Biology Organization 2003
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container_issue	11
title_short	Epigenetic consequences of AML1–ETO action at the human c‐FMS locus
url	https://dx.doi.org/10.1093/emboj/cdg250
remote_bool	true
author2	Tagoh, Hiromi Lefevre, Pascal Hodge, Donald Morgan, Gareth J. Bonifer, Constanze
author2Str	Tagoh, Hiromi Lefevre, Pascal Hodge, Donald Morgan, Gareth J. Bonifer, Constanze
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doi_str	10.1093/emboj/cdg250
up_date	2024-10-24T04:55:55.043Z
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Epigenetic consequences of AML1–ETO action at the human c‐FMS locus

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