Source:http://linkedlifedata.com/resource/pubmed/id/12351384
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
|
pubmed:dateCreated |
2002-9-27
|
pubmed:abstractText |
In the search for genes expressed in hematopoietic stem cells, we identified that the expression of Gfi-1B (growth factor independence-1B) is highly restricted to hematopoietic stem cells, erythroblasts, and megakaryocytes. Gfi-1 and Gfi-1B are zinc finger proteins that share highly conserved SNAG and 6 zinc finger domains. Gfi-1 has been characterized as an oncogene involved in lymphoid malignancies in mice. In contrast, role of Gfi-1B in hematopoiesis has not been well characterized. In this study, we analyzed its function in human hematopoiesis. Enforced expression of Gfi-1B in human CD34(+) hematopoietic progenitors induced a drastic expansion of erythroblasts in an erythropoietin-independent manner. Expression of Gfi-1B did not promote erythroid commitment, but enhanced proliferation of immature erythroblasts. Erythroblasts expanded by exogenous Gfi-1B, however, failed to differentiate beyond proerythroblast stage and showed massive apoptosis. These biologic effects of Gfi-1B were mediated through its zinc finger domain, but not by the SNAG or non-zinc finger domain. Proliferation of erythroblasts was associated with sustained expression of GATA-2 but not of GATA-1, indicating a potential link between Gfi-1B and GATA family regulators. Importantly, the function of Gfi-1B to modulate transcription was dependent on promoter context. In addition, activation of transcription of an artificial promoter was mediated through its zinc finger domain. These findings establish Gfi-1B as a novel erythroid regulator and reveal its specific involvement in the regulation of erythroid cell growth through modulating erythroid-specific gene expression.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/GFI1B protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Gfi1b protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0006-4971
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
100
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2769-77
|
pubmed:dateRevised |
2004-11-18
|
pubmed:meshHeading |
pubmed-meshheading:12351384-Animals,
pubmed-meshheading:12351384-Base Sequence,
pubmed-meshheading:12351384-Cell Culture Techniques,
pubmed-meshheading:12351384-Cells, Cultured,
pubmed-meshheading:12351384-Colony-Forming Units Assay,
pubmed-meshheading:12351384-Conserved Sequence,
pubmed-meshheading:12351384-DNA Primers,
pubmed-meshheading:12351384-Erythroblasts,
pubmed-meshheading:12351384-Erythropoiesis,
pubmed-meshheading:12351384-Flow Cytometry,
pubmed-meshheading:12351384-Gene Expression Regulation,
pubmed-meshheading:12351384-Hematopoiesis,
pubmed-meshheading:12351384-Hematopoietic Stem Cells,
pubmed-meshheading:12351384-Humans,
pubmed-meshheading:12351384-Megakaryocytes,
pubmed-meshheading:12351384-Mice,
pubmed-meshheading:12351384-Proto-Oncogene Proteins,
pubmed-meshheading:12351384-Repressor Proteins,
pubmed-meshheading:12351384-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:12351384-Zinc Fingers
|
pubmed:year |
2002
|
pubmed:articleTitle |
Erythroid expansion mediated by the Gfi-1B zinc finger protein: role in normal hematopoiesis.
|
pubmed:affiliation |
Department of Immunology, Institute of Basic Medical Sciences, University of Tsukuba, and Core Research for Evolutional Science and Technology of Japan Science and Technology, Japan.
|
pubmed:publicationType |
Journal Article
|