Source:http://linkedlifedata.com/resource/pubmed/id/10421778
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1999-9-24
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pubmed:abstractText |
While Jun/Fos-containing transcription factors are known to be necessary for many TCR-mediated events in mature T cells, relatively little is known about their roles in thymocyte development. We have generated transgenic mice that express a trans-dominant-negative mutant of c-Jun (TAM-67) specifically in thymocytes. Expression of TAM-67 inhibited the up-regulation of AP-1-responsive genes such as c-jun and IL-2 in stimulated thymocytes from transgenic mice. In addition, altered thymocyte development in TAM-67-expressing mice was revealed by a decrease in thymic cellularity ( approximately 50%) which could be accounted for primarily by a reduction in the number of CD4(+)CD8(+) thymocytes, a large percentage of which retained CD25. The decrease in the number of CD4(+)CD8(+) thymocytes did not appear to be due to an enhanced rate of apoptosis but rather to a decrease in the number of CD4(-)CD8(-)CD25(-) cells in the S + G(2)/M stages of the cell cycle. These results indicate that Jun/Fos-containing transcription factors promote the proliferative burst that accompanies the transition from the CD4(-)CD8(-) to the CD4(+)CD8(+) stage of thymocyte development.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0953-8178
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1203-16
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10421778-Animals,
pubmed-meshheading:10421778-CD4-Positive T-Lymphocytes,
pubmed-meshheading:10421778-CD8-Positive T-Lymphocytes,
pubmed-meshheading:10421778-Cell Cycle,
pubmed-meshheading:10421778-Cell Differentiation,
pubmed-meshheading:10421778-Gene Expression Regulation, Developmental,
pubmed-meshheading:10421778-Genes, jun,
pubmed-meshheading:10421778-Interleukin-2,
pubmed-meshheading:10421778-Lymphocyte Activation,
pubmed-meshheading:10421778-Mice,
pubmed-meshheading:10421778-Mice, Inbred C57BL,
pubmed-meshheading:10421778-Mice, Inbred DBA,
pubmed-meshheading:10421778-Mice, Knockout,
pubmed-meshheading:10421778-Mice, Transgenic,
pubmed-meshheading:10421778-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:10421778-Receptors, Interleukin-2,
pubmed-meshheading:10421778-T-Lymphocyte Subsets,
pubmed-meshheading:10421778-Thymus Gland,
pubmed-meshheading:10421778-Transcription Factor AP-1,
pubmed-meshheading:10421778-Transcription Factors
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pubmed:year |
1999
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pubmed:articleTitle |
A dominant-negative mutant of c-Jun inhibits cell cycle progression during the transition of CD4(-)CD8(-) to CD4(+)CD8(+) thymocytes.
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pubmed:affiliation |
Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda MD 20892, 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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