Elucidation of the role of LMO2 in human erythroid cells
LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Inoue, Ai [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013transfer abstract |
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| Umfang: |
9700 |
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| Übergeordnetes Werk: |
Enthalten in: Interfacing 2D M - Rawat, Ashima ELSEVIER, 2021, official publication of the International Society for Experimental Hematology, Amsterdam [u.a] |
|---|---|
| Übergeordnetes Werk: |
volume:41 ; year:2013 ; number:12 ; pages:1062-10761 ; extent:9700 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.exphem.2013.09.003 |
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ELV021866376 |
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| 245 | 1 | 0 | |a Elucidation of the role of LMO2 in human erythroid cells |
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| 520 | |a LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. | ||
| 520 | |a LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. | ||
| 700 | 1 | |a Fujiwara, Tohru |4 oth | |
| 700 | 1 | |a Okitsu, Yoko |4 oth | |
| 700 | 1 | |a Katsuoka, Yuna |4 oth | |
| 700 | 1 | |a Fukuhara, Noriko |4 oth | |
| 700 | 1 | |a Onishi, Yasushi |4 oth | |
| 700 | 1 | |a Ishizawa, Kenichi |4 oth | |
| 700 | 1 | |a Harigae, Hideo |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Rawat, Ashima ELSEVIER |t Interfacing 2D M |d 2021 |d official publication of the International Society for Experimental Hematology |g Amsterdam [u.a] |w (DE-627)ELV006315852 |
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| 856 | 4 | 0 | |u https://doi.org/10.1016/j.exphem.2013.09.003 |3 Volltext |
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2013 |
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10.1016/j.exphem.2013.09.003 doi GBVA2013009000025.pica (DE-627)ELV021866376 (ELSEVIER)S0301-472X(13)00706-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 530 660 VZ 33.68 bkl 35.18 bkl 52.78 bkl Inoue, Ai verfasserin aut Elucidation of the role of LMO2 in human erythroid cells 2013transfer abstract 9700 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. Fujiwara, Tohru oth Okitsu, Yoko oth Katsuoka, Yuna oth Fukuhara, Noriko oth Onishi, Yasushi oth Ishizawa, Kenichi oth Harigae, Hideo oth Enthalten in Elsevier Science Rawat, Ashima ELSEVIER Interfacing 2D M 2021 official publication of the International Society for Experimental Hematology Amsterdam [u.a] (DE-627)ELV006315852 volume:41 year:2013 number:12 pages:1062-10761 extent:9700 https://doi.org/10.1016/j.exphem.2013.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 33.68 Oberflächen Dünne Schichten Grenzflächen Physik VZ 35.18 Kolloidchemie Grenzflächenchemie VZ 52.78 Oberflächentechnik Wärmebehandlung VZ AR 41 2013 12 1062-10761 9700 045F 610 |
| spelling |
10.1016/j.exphem.2013.09.003 doi GBVA2013009000025.pica (DE-627)ELV021866376 (ELSEVIER)S0301-472X(13)00706-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 530 660 VZ 33.68 bkl 35.18 bkl 52.78 bkl Inoue, Ai verfasserin aut Elucidation of the role of LMO2 in human erythroid cells 2013transfer abstract 9700 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. Fujiwara, Tohru oth Okitsu, Yoko oth Katsuoka, Yuna oth Fukuhara, Noriko oth Onishi, Yasushi oth Ishizawa, Kenichi oth Harigae, Hideo oth Enthalten in Elsevier Science Rawat, Ashima ELSEVIER Interfacing 2D M 2021 official publication of the International Society for Experimental Hematology Amsterdam [u.a] (DE-627)ELV006315852 volume:41 year:2013 number:12 pages:1062-10761 extent:9700 https://doi.org/10.1016/j.exphem.2013.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 33.68 Oberflächen Dünne Schichten Grenzflächen Physik VZ 35.18 Kolloidchemie Grenzflächenchemie VZ 52.78 Oberflächentechnik Wärmebehandlung VZ AR 41 2013 12 1062-10761 9700 045F 610 |
| allfields_unstemmed |
10.1016/j.exphem.2013.09.003 doi GBVA2013009000025.pica (DE-627)ELV021866376 (ELSEVIER)S0301-472X(13)00706-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 530 660 VZ 33.68 bkl 35.18 bkl 52.78 bkl Inoue, Ai verfasserin aut Elucidation of the role of LMO2 in human erythroid cells 2013transfer abstract 9700 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. Fujiwara, Tohru oth Okitsu, Yoko oth Katsuoka, Yuna oth Fukuhara, Noriko oth Onishi, Yasushi oth Ishizawa, Kenichi oth Harigae, Hideo oth Enthalten in Elsevier Science Rawat, Ashima ELSEVIER Interfacing 2D M 2021 official publication of the International Society for Experimental Hematology Amsterdam [u.a] (DE-627)ELV006315852 volume:41 year:2013 number:12 pages:1062-10761 extent:9700 https://doi.org/10.1016/j.exphem.2013.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 33.68 Oberflächen Dünne Schichten Grenzflächen Physik VZ 35.18 Kolloidchemie Grenzflächenchemie VZ 52.78 Oberflächentechnik Wärmebehandlung VZ AR 41 2013 12 1062-10761 9700 045F 610 |
| allfieldsGer |
10.1016/j.exphem.2013.09.003 doi GBVA2013009000025.pica (DE-627)ELV021866376 (ELSEVIER)S0301-472X(13)00706-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 670 530 660 VZ 33.68 bkl 35.18 bkl 52.78 bkl Inoue, Ai verfasserin aut Elucidation of the role of LMO2 in human erythroid cells 2013transfer abstract 9700 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. Fujiwara, Tohru oth Okitsu, Yoko oth Katsuoka, Yuna oth Fukuhara, Noriko oth Onishi, Yasushi oth Ishizawa, Kenichi oth Harigae, Hideo oth Enthalten in Elsevier Science Rawat, Ashima ELSEVIER Interfacing 2D M 2021 official publication of the International Society for Experimental Hematology Amsterdam [u.a] (DE-627)ELV006315852 volume:41 year:2013 number:12 pages:1062-10761 extent:9700 https://doi.org/10.1016/j.exphem.2013.09.003 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 33.68 Oberflächen Dünne Schichten Grenzflächen Physik VZ 35.18 Kolloidchemie Grenzflächenchemie VZ 52.78 Oberflächentechnik Wärmebehandlung VZ AR 41 2013 12 1062-10761 9700 045F 610 |
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Elucidation of the role of LMO2 in human erythroid cells |
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LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. |
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LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. |
| abstract_unstemmed |
LIM-only protein 2 (LMO2) is a non–DNA-binding component of a protein complex containing master regulators of hematopoiesis, including GATA-1, SCL/TAL1, and LDB1. However, the role of LMO2 in human erythroid differentiation is unclear. LMO2 knockdown in hemin-treated K562 cells reduced the benzidine-positive cell ratio, suggesting that LMO2 retards hemin-mediated K562 cell differentiation. Microarray analysis using K562 cells after siRNA-mediated LMO2 knockdown indicated that 177 and 78 genes were upregulated and downregulated (>1.5-fold), respectively. The downregulated gene ensemble contained prototypical erythroid genes (HBB, SLC4A1). Whereas LMO2 knockdown did not affect GATA-1 or SCL/TAL1 expression, it resulted in significantly reduced chromatin occupancy of GATA-1, SCL/TAL1, and LDB1 at the β-globin locus control region and SLC4A1 locus in both K562 cells and human induced pluripotent stem cell–derived erythroid cells. Introduction of GATA-1 mutations, shown to impair direct interaction with LMO2, significantly diminished chromatin occupancy. On the other hand, knockdown of either SCL/TAL1 or LDB1 also resulted in significantly reduced chromatin occupancy of GATA-1 at endogenous loci, suggesting that impaired assembly of these components also affects GATA-1 chromatin occupancy. In an ex vivo model of erythroid differentiation from CD34+ cells, LMO2 protein level peaked on day 5 and decreased at later stages of differentiation. The LMO2 expression pattern was similar to those of GATA-1 and SCL/TAL1. Furthermore, shRNA-mediated LMO2 knockdown in primary erythroblasts suggested that LMO2 regulates HBB, HBA, and SLC4A1 expression. LMO2 contributes to GATA-1 target gene expression by affecting assembly of the GATA-SCL/TAL1 complex components at endogenous loci. |
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| title_short |
Elucidation of the role of LMO2 in human erythroid cells |
| url |
https://doi.org/10.1016/j.exphem.2013.09.003 |
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| author2 |
Fujiwara, Tohru Okitsu, Yoko Katsuoka, Yuna Fukuhara, Noriko Onishi, Yasushi Ishizawa, Kenichi Harigae, Hideo |
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Fujiwara, Tohru Okitsu, Yoko Katsuoka, Yuna Fukuhara, Noriko Onishi, Yasushi Ishizawa, Kenichi Harigae, Hideo |
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10.1016/j.exphem.2013.09.003 |
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2024-07-06T20:38:12.434Z |
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