Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-5-8
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
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
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6091-8
pubmed:dateRevised
2007-11-14
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
pubmed:year
2001
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.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't