Source:http://linkedlifedata.com/resource/pubmed/id/15507521
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2005-2-3
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pubmed:abstractText |
Growth factor independence-1B (Gfi-1B) is a transcription factor with a highly conserved transcriptional repressor snail-Gfi-1 (SNAG) domain and 6 zinc-finger domains at the N- and C-terminus, respectively. Disruption of the Gfi-1B gene is lethal in the embryo with failure to produce definitive enucleated erythrocytes. In this study, we analyzed the role of Gfi-1B in human erythropoiesis. We observed an increase of Gfi-1B expression during erythroid maturation of human primary progenitor cells. We studied the consequences of variations in Gfi-1B expression in 2 transformed cell lines (K562 and UT7 cells), as well as in primary CD36(+)/GPA(-) progenitors. A knock-down of Gfi-1B delayed the terminal differentiation of K562 and primary cells. Forced expression of Gfi-1B in UT7 and K562 cells led to an arrest of proliferation and an induction of erythroid differentiation. Enforced expression of Gfi-1B in primary cells at the colony-forming units-erythroid (CFU-E) stage led to a partial glycophorin A (GPA) induction after erythropoietin (EPO) withdrawal but failed to protect cells from apoptosis. Deletion of the SNAG repressor domain abolished Gfi-1B-induced erythroid maturation, strongly suggesting that Gfi-1B acts in the late stage of erythroid differentiation as a transcriptional repressor.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD36,
http://linkedlifedata.com/resource/pubmed/chemical/Erythropoietin,
http://linkedlifedata.com/resource/pubmed/chemical/GFI1B protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0006-4971
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
105
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1448-55
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15507521-Antigens, CD36,
pubmed-meshheading:15507521-Cell Differentiation,
pubmed-meshheading:15507521-Cell Line, Tumor,
pubmed-meshheading:15507521-Cell Proliferation,
pubmed-meshheading:15507521-Cell Transformation, Neoplastic,
pubmed-meshheading:15507521-Cells, Cultured,
pubmed-meshheading:15507521-Down-Regulation,
pubmed-meshheading:15507521-Erythroid Precursor Cells,
pubmed-meshheading:15507521-Erythropoietin,
pubmed-meshheading:15507521-Gene Silencing,
pubmed-meshheading:15507521-Humans,
pubmed-meshheading:15507521-K562 Cells,
pubmed-meshheading:15507521-Protein Structure, Tertiary,
pubmed-meshheading:15507521-Proto-Oncogene Proteins,
pubmed-meshheading:15507521-RNA, Small Interfering,
pubmed-meshheading:15507521-Repressor Proteins,
pubmed-meshheading:15507521-Transfection,
pubmed-meshheading:15507521-Up-Regulation
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pubmed:year |
2005
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pubmed:articleTitle |
Gfi-1B plays a critical role in terminal differentiation of normal and transformed erythroid progenitor cells.
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pubmed:affiliation |
Institut National de la Santé et de la Recherche Médicale (INSERM) U362, Institut Gustave Roussy, 94805 Villejuif cedex, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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