Abstract
NF-κB/Rel designates a widely distributed family of transcription factors involved in immune and acute phase responses. Here, the expression and function of NF-κB factors in erythroid proliferation and differentiation were explored. In an erythroleukemia cell line, TF-1, high levels of p105/p50, p100/p52, p65, and IκBα were detected 24 hours after growth factor deprivation. In response to granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation, significant induction of p52 expression was observed. GM-CSF also induced nuclear translocation of both p52 and p65. No induction of NF-κB factors was observed with erythropoietin stimulation of TF-1 cells. Overexpression of p52 and p65 in TF-1 cells by transient transfection resulted in significant induction of a κB-TATA-luciferase reporter plasmid, showing that these factors are functional in vivo in erythroid cells. To determine whether NF-κB factors may play a role in normal erythropoiesis, levels of these factors were determined in burst- forming unit-erythroid (BFU-E)derived cells at different stages of differentiation. The NF-κB factors p105/p50, p100/p52, and p65 were highly expressed in early BFU-E-derived precursors, which are rapidly proliferating, and declined during maturation. Furthermore, nuclear levels of NF-κB factors p50, p52, and p65 were higher in less mature precursors (day 10 BFU-E- derived cells) compared with more differentiated (day 14) erythroblasts. In nuclear extracts from day 10 BFU-E-derived cells, p50, p52, and p65 were able to form complexes, which bound to κB sites in the promoters of both the c- myb and c-myc genes, suggesting that c-myb and c-myc may be among the κB- containing genes regulated by NF-κB factors in normal erythroid cells. Taken together, these data show that NF-κB factors are modulated by GM-CSF and suggest they function to regulate specific KB containing genes involved in erythropoiesis.
Original language | English (US) |
---|---|
Pages (from-to) | 4136-4144 |
Number of pages | 9 |
Journal | Blood |
Volume | 91 |
Issue number | 11 |
DOIs | |
State | Published - Jun 1 1998 |
Externally published | Yes |
ASJC Scopus subject areas
- Biochemistry
- Immunology
- Hematology
- Cell Biology
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Zhang, M. Y., Sun, S. C., Bell, L., & Miller, B. A. (1998). NF-κB transcription factors are involved in normal erythropoiesis. Blood, 91(11), 4136-4144. https://doi.org/10.1182/blood.v91.11.4136
NF-κB transcription factors are involved in normal erythropoiesis. / Zhang, Min Ying; Sun, Shao Cong; Bell, Laurie et al.
In: Blood, Vol. 91, No. 11, 01.06.1998, p. 4136-4144.
Research output: Contribution to journal › Article › peer-review
Zhang, MY, Sun, SC, Bell, L & Miller, BA 1998, 'NF-κB transcription factors are involved in normal erythropoiesis', Blood, vol. 91, no. 11, pp. 4136-4144. https://doi.org/10.1182/blood.v91.11.4136
Zhang MY, Sun SC, Bell L, Miller BA. NF-κB transcription factors are involved in normal erythropoiesis. Blood. 1998 Jun 1;91(11):4136-4144. doi: 10.1182/blood.v91.11.4136
Zhang, Min Ying ; Sun, Shao Cong ; Bell, Laurie et al. / NF-κB transcription factors are involved in normal erythropoiesis. In: Blood. 1998 ; Vol. 91, No. 11. pp. 4136-4144.
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title = "NF-κB transcription factors are involved in normal erythropoiesis",
abstract = "NF-κB/Rel designates a widely distributed family of transcription factors involved in immune and acute phase responses. Here, the expression and function of NF-κB factors in erythroid proliferation and differentiation were explored. In an erythroleukemia cell line, TF-1, high levels of p105/p50, p100/p52, p65, and IκBα were detected 24 hours after growth factor deprivation. In response to granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation, significant induction of p52 expression was observed. GM-CSF also induced nuclear translocation of both p52 and p65. No induction of NF-κB factors was observed with erythropoietin stimulation of TF-1 cells. Overexpression of p52 and p65 in TF-1 cells by transient transfection resulted in significant induction of a κB-TATA-luciferase reporter plasmid, showing that these factors are functional in vivo in erythroid cells. To determine whether NF-κB factors may play a role in normal erythropoiesis, levels of these factors were determined in burst- forming unit-erythroid (BFU-E)derived cells at different stages of differentiation. The NF-κB factors p105/p50, p100/p52, and p65 were highly expressed in early BFU-E-derived precursors, which are rapidly proliferating, and declined during maturation. Furthermore, nuclear levels of NF-κB factors p50, p52, and p65 were higher in less mature precursors (day 10 BFU-E- derived cells) compared with more differentiated (day 14) erythroblasts. In nuclear extracts from day 10 BFU-E-derived cells, p50, p52, and p65 were able to form complexes, which bound to κB sites in the promoters of both the c- myb and c-myc genes, suggesting that c-myb and c-myc may be among the κB- containing genes regulated by NF-κB factors in normal erythroid cells. Taken together, these data show that NF-κB factors are modulated by GM-CSF and suggest they function to regulate specific KB containing genes involved in erythropoiesis.",
author = "Zhang, {Min Ying} and Sun, {Shao Cong} and Laurie Bell and Miller, {Barbara A.}",
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T1 - NF-κB transcription factors are involved in normal erythropoiesis
AU - Zhang, Min Ying
AU - Sun, Shao Cong
AU - Bell, Laurie
AU - Miller, Barbara A.
PY - 1998/6/1
Y1 - 1998/6/1
N2 - NF-κB/Rel designates a widely distributed family of transcription factors involved in immune and acute phase responses. Here, the expression and function of NF-κB factors in erythroid proliferation and differentiation were explored. In an erythroleukemia cell line, TF-1, high levels of p105/p50, p100/p52, p65, and IκBα were detected 24 hours after growth factor deprivation. In response to granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation, significant induction of p52 expression was observed. GM-CSF also induced nuclear translocation of both p52 and p65. No induction of NF-κB factors was observed with erythropoietin stimulation of TF-1 cells. Overexpression of p52 and p65 in TF-1 cells by transient transfection resulted in significant induction of a κB-TATA-luciferase reporter plasmid, showing that these factors are functional in vivo in erythroid cells. To determine whether NF-κB factors may play a role in normal erythropoiesis, levels of these factors were determined in burst- forming unit-erythroid (BFU-E)derived cells at different stages of differentiation. The NF-κB factors p105/p50, p100/p52, and p65 were highly expressed in early BFU-E-derived precursors, which are rapidly proliferating, and declined during maturation. Furthermore, nuclear levels of NF-κB factors p50, p52, and p65 were higher in less mature precursors (day 10 BFU-E- derived cells) compared with more differentiated (day 14) erythroblasts. In nuclear extracts from day 10 BFU-E-derived cells, p50, p52, and p65 were able to form complexes, which bound to κB sites in the promoters of both the c- myb and c-myc genes, suggesting that c-myb and c-myc may be among the κB- containing genes regulated by NF-κB factors in normal erythroid cells. Taken together, these data show that NF-κB factors are modulated by GM-CSF and suggest they function to regulate specific KB containing genes involved in erythropoiesis.
AB - NF-κB/Rel designates a widely distributed family of transcription factors involved in immune and acute phase responses. Here, the expression and function of NF-κB factors in erythroid proliferation and differentiation were explored. In an erythroleukemia cell line, TF-1, high levels of p105/p50, p100/p52, p65, and IκBα were detected 24 hours after growth factor deprivation. In response to granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulation, significant induction of p52 expression was observed. GM-CSF also induced nuclear translocation of both p52 and p65. No induction of NF-κB factors was observed with erythropoietin stimulation of TF-1 cells. Overexpression of p52 and p65 in TF-1 cells by transient transfection resulted in significant induction of a κB-TATA-luciferase reporter plasmid, showing that these factors are functional in vivo in erythroid cells. To determine whether NF-κB factors may play a role in normal erythropoiesis, levels of these factors were determined in burst- forming unit-erythroid (BFU-E)derived cells at different stages of differentiation. The NF-κB factors p105/p50, p100/p52, and p65 were highly expressed in early BFU-E-derived precursors, which are rapidly proliferating, and declined during maturation. Furthermore, nuclear levels of NF-κB factors p50, p52, and p65 were higher in less mature precursors (day 10 BFU-E- derived cells) compared with more differentiated (day 14) erythroblasts. In nuclear extracts from day 10 BFU-E-derived cells, p50, p52, and p65 were able to form complexes, which bound to κB sites in the promoters of both the c- myb and c-myc genes, suggesting that c-myb and c-myc may be among the κB- containing genes regulated by NF-κB factors in normal erythroid cells. Taken together, these data show that NF-κB factors are modulated by GM-CSF and suggest they function to regulate specific KB containing genes involved in erythropoiesis.
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