The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia

Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Wilcher, Katherine E. [verfasserIn] Page, Evan R.H. [verfasserIn] Privette Vinnedge, Lisa M. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Übergeordnetes Werk:	Enthalten in: Experimental hematology - Amsterdam [u.a] : Elsevier Science, 2011, 123, Seite 18-27
Übergeordnetes Werk:	volume:123 ; pages:18-27

DOI / URN:	10.1016/j.exphem.2023.05.002

Katalog-ID:	ELV059944587

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245	1	0	\|a The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
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520			\|a Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors.
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700	1		\|a Privette Vinnedge, Lisa M. \|e verfasserin \|4 aut
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author_variant	k e w ke kew e r p er erp v l m p vlm vlmp
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allfields	10.1016/j.exphem.2023.05.002 doi (DE-627)ELV059944587 (ELSEVIER)S0301-472X(23)00225-4 DE-627 ger DE-627 rda eng 610 VZ Wilcher, Katherine E. verfasserin aut The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors. Page, Evan R.H. verfasserin aut Privette Vinnedge, Lisa M. verfasserin aut Enthalten in Experimental hematology Amsterdam [u.a] : Elsevier Science, 2011 123, Seite 18-27 (DE-627)320445291 (DE-600)2005403-8 187-32399 nnns volume:123 pages:18-27 GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 123 18-27
spelling	10.1016/j.exphem.2023.05.002 doi (DE-627)ELV059944587 (ELSEVIER)S0301-472X(23)00225-4 DE-627 ger DE-627 rda eng 610 VZ Wilcher, Katherine E. verfasserin aut The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors. Page, Evan R.H. verfasserin aut Privette Vinnedge, Lisa M. verfasserin aut Enthalten in Experimental hematology Amsterdam [u.a] : Elsevier Science, 2011 123, Seite 18-27 (DE-627)320445291 (DE-600)2005403-8 187-32399 nnns volume:123 pages:18-27 GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 123 18-27
allfields_unstemmed	10.1016/j.exphem.2023.05.002 doi (DE-627)ELV059944587 (ELSEVIER)S0301-472X(23)00225-4 DE-627 ger DE-627 rda eng 610 VZ Wilcher, Katherine E. verfasserin aut The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors. Page, Evan R.H. verfasserin aut Privette Vinnedge, Lisa M. verfasserin aut Enthalten in Experimental hematology Amsterdam [u.a] : Elsevier Science, 2011 123, Seite 18-27 (DE-627)320445291 (DE-600)2005403-8 187-32399 nnns volume:123 pages:18-27 GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 123 18-27
allfieldsGer	10.1016/j.exphem.2023.05.002 doi (DE-627)ELV059944587 (ELSEVIER)S0301-472X(23)00225-4 DE-627 ger DE-627 rda eng 610 VZ Wilcher, Katherine E. verfasserin aut The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors. Page, Evan R.H. verfasserin aut Privette Vinnedge, Lisa M. verfasserin aut Enthalten in Experimental hematology Amsterdam [u.a] : Elsevier Science, 2011 123, Seite 18-27 (DE-627)320445291 (DE-600)2005403-8 187-32399 nnns volume:123 pages:18-27 GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 123 18-27
allfieldsSound	10.1016/j.exphem.2023.05.002 doi (DE-627)ELV059944587 (ELSEVIER)S0301-472X(23)00225-4 DE-627 ger DE-627 rda eng 610 VZ Wilcher, Katherine E. verfasserin aut The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors. Page, Evan R.H. verfasserin aut Privette Vinnedge, Lisa M. verfasserin aut Enthalten in Experimental hematology Amsterdam [u.a] : Elsevier Science, 2011 123, Seite 18-27 (DE-627)320445291 (DE-600)2005403-8 187-32399 nnns volume:123 pages:18-27 GBV_USEFLAG_U GBV_ELV SYSFLAG_U GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 123 18-27
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author	Wilcher, Katherine E.
spellingShingle	Wilcher, Katherine E. ddc 610 The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
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topic_title	610 VZ The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
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title	The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
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title_full	The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
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title_sort	the impact of the chromatin binding dek protein in hematopoiesis and acute myeloid leukemia
title_auth	The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
abstract	Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors.
abstractGer	Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors.
abstract_unstemmed	Hematopoiesis is an exquisitely regulated process of cellular differentiation to create diverse cell types of the blood. Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors.
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title_short	The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia
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up_date	2024-07-06T23:23:59.338Z
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Genetic mutations, or aberrant regulation of gene transcription, can interrupt normal hematopoiesis. This can have dire pathological consequences, including acute myeloid leukemia (AML), in which generation of the myeloid lineage of differentiated cells is interrupted. In this literature review, we discuss how the chromatin remodeling DEK protein can control hematopoietic stem cell quiescence, hematopoietic progenitor cell proliferation, and myelopoiesis. We further discuss the oncogenic consequences of the t(6;9) chromosomal translocation, which creates the DEK-NUP214 (aka: DEK-CAN) fusion gene, during the pathogenesis of AML. Combined, the literature indicates that DEK is crucial for maintaining homeostasis of hematopoietic stem and progenitor cells, including myeloid progenitors.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Page, Evan R.H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Privette Vinnedge, Lisa M.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Experimental hematology</subfield><subfield code="d">Amsterdam [u.a] : Elsevier Science, 2011</subfield><subfield code="g">123, Seite 18-27</subfield><subfield code="w">(DE-627)320445291</subfield><subfield code="w">(DE-600)2005403-8</subfield><subfield code="x">187-32399</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" 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The impact of the chromatin binding DEK protein in hematopoiesis and acute myeloid leukemia

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