NF-κB transcription factors are involved in normal erythropoiesis (2023)

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 languageEnglish (US)
Pages (from-to)4136-4144
Number of pages9
JournalBlood
Volume91
Issue number11
DOIs
StatePublished - Jun 1 1998
Externally publishedYes

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 journalArticlepeer-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.

@article{d8d5f38e6b5a4634b766f95b73d3f980,

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.",

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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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