rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2001-5-8
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pubmed:abstractText |
During early B lymphopoiesis, developing B cells maintain lineage commitment despite the local presence of myeloid lineage-promoting cytokines such as GM-CSF and IL-3. Previous observations suggest that the B cell-specific transcription factor Pax5A (paired box 5A transcription factor) plays a role in maintaining B cell lineage commitment by limiting expansion and survival of early IL-3/GM-CSF-dependent myeloid lineage cells. To define a mechanism by which Pax5A can exert these inhibitory effects on myeloid lineage differentiation, an inducible form of the Pax5A protein was expressed in the myeloid cell line FDC-P1. This cell line models myeloid progenitors in that it responds to the survival and growth-potentiating effects of IL-3 and GM-CSF. We observed that enforced expression of Pax5A selectively suppressed proliferation in response to GM-CSF, but not IL-3. This effect was associated with specific down-regulation of GM-CSFR alpha-chain, but not beta-chain expression. These data provide a molecular mechanism to enforce commitment to the B cell lineage despite the presence of GM-CSF, a factor that has been shown to convert early developing B cells to the myeloid lineage. Furthermore, they indicate a role for B cell Pax5A expression in maintaining rather than directing commitment to the B cell lineage.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/B-Cell-Specific Activator Protein,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte-Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-3,
http://linkedlifedata.com/resource/pubmed/chemical/PAX5 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Pax5 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Drug,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Granulocyte-Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Tamoxifen,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
166
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6091-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11342627-Animals,
pubmed-meshheading:11342627-B-Cell-Specific Activator Protein,
pubmed-meshheading:11342627-B-Lymphocytes,
pubmed-meshheading:11342627-Cell Differentiation,
pubmed-meshheading:11342627-Cell Line,
pubmed-meshheading:11342627-Cell Line, Transformed,
pubmed-meshheading:11342627-Cell Lineage,
pubmed-meshheading:11342627-DNA-Binding Proteins,
pubmed-meshheading:11342627-Gene Expression Regulation,
pubmed-meshheading:11342627-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:11342627-Growth Inhibitors,
pubmed-meshheading:11342627-Humans,
pubmed-meshheading:11342627-Interleukin-3,
pubmed-meshheading:11342627-Mice,
pubmed-meshheading:11342627-Proteins,
pubmed-meshheading:11342627-Receptors, Drug,
pubmed-meshheading:11342627-Receptors, Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:11342627-Stem Cells,
pubmed-meshheading:11342627-Tamoxifen,
pubmed-meshheading:11342627-Transcription Factors,
pubmed-meshheading:11342627-Tumor Cells, Cultured
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pubmed:year |
2001
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pubmed:articleTitle |
Role for transcription Pax5A factor in maintaining commitment to the B cell lineage by selective inhibition of granulocyte-macrophage colony-stimulating factor receptor expression.
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pubmed:affiliation |
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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