pubmed-article:12133947 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0038250 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0005953 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0082978 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0220905 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C1881379 | lld:lifeskim |
pubmed-article:12133947 | lifeskim:mentions | umls-concept:C0181090 | lld:lifeskim |
pubmed-article:12133947 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:12133947 | pubmed:dateCreated | 2002-7-22 | lld:pubmed |
pubmed-article:12133947 | pubmed:abstractText | IFN consensus sequence binding protein (ICSBP; IFN regulatory factor-8) is a transcription factor of the IFN regulatory factor family. Disruption of this gene results in a leukemia-like disease in mice. To investigate the role of ICSBP in myeloid cell development, lineage marker-negative (Lin(-)) bone marrow progenitor cells were purified from ICSBP(+/+) and ICSBP(-/-) mice and tested for gene expression and colony-forming ability. ICSBP was expressed in Lin(-) progenitor cells, and its levels were markedly increased by IFN-gamma. The colony-forming potential of ICSBP(-/-) progenitor cells was grossly abnormal, as they gave rise to a disproportionately high number of granulocyte colonies and many fewer macrophage colonies. IFN-gamma inhibited colony formation, while promoting macrophage maturation in ICSBP(+/+) cells. In contrast, the effects of IFN-gamma were completely absent in ICSBP(-/-) progenitors. By retrovirus transduction we tested whether reintroduction of ICSBP restores a normal colony-forming potential in -/- progenitor cells. The wild-type ICSBP, but not transcriptionally defective mutants, corrected abnormal colony formation by increasing macrophage colonies and decreasing granulocyte colonies. Taken together, ICSBP plays a critical role in myeloid cell development by controlling lineage selection and is indispensable for IFN-gamma-dependent modulation of progenitor cell maturation. | lld:pubmed |
pubmed-article:12133947 | pubmed:language | eng | lld:pubmed |
pubmed-article:12133947 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12133947 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:12133947 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12133947 | pubmed:month | Aug | lld:pubmed |
pubmed-article:12133947 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:12133947 | pubmed:author | pubmed-author:OzatoKeikoK | lld:pubmed |
pubmed-article:12133947 | pubmed:author | pubmed-author:TamuraTomohik... | lld:pubmed |
pubmed-article:12133947 | pubmed:author | pubmed-author:TsujimuraHide... | lld:pubmed |
pubmed-article:12133947 | pubmed:author | pubmed-author:Nagamura-Inou... | lld:pubmed |
pubmed-article:12133947 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12133947 | pubmed:day | 1 | lld:pubmed |
pubmed-article:12133947 | pubmed:volume | 169 | lld:pubmed |
pubmed-article:12133947 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12133947 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12133947 | pubmed:pagination | 1261-9 | lld:pubmed |
pubmed-article:12133947 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:12133947 | pubmed:meshHeading | pubmed-meshheading:12133947... | lld:pubmed |
pubmed-article:12133947 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12133947 | pubmed:articleTitle | IFN consensus sequence binding protein/IFN regulatory factor-8 guides bone marrow progenitor cells toward the macrophage lineage. | lld:pubmed |
pubmed-article:12133947 | pubmed:affiliation | Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. | lld:pubmed |
pubmed-article:12133947 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12133947 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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