Source:http://linkedlifedata.com/resource/pubmed/id/12039915
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2002-5-31
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| pubmed:abstractText |
The transcription factor recombination signal binding protein-J (RBP-J) functions immediately downstream of the cell surface receptor Notch and mediates transcriptional activation by the intracellular domain of all four kinds of Notch receptors. To investigate the function of RBP-J, we introduced loxP sites on both sides of the RBP-J exons encoding its DNA binding domain. Mice bearing the loxP-flanked RBP-J alleles, RBP-J(f/f), were mated with Mx-Cre transgenic mice and deletional mutation of the RBP-J gene in adult mice was induced by injection of the IFN-alpha inducer poly(I)-poly(C). Here we show that inactivation of RBP-J in bone marrow resulted in a block of T cell development at the earliest stage and increase of B cell development in the thymus. Lymphoid progenitors deficient in RBP-J differentiate into B but not T cells when cultured in 2'-deoxyguanosine-treated fetal thymic lobes by hanging-drop fetal thymus organ culture. Competitive repopulation assay also revealed cell autonomous deficiency of T cell development from bone marrow of RBP-J knockout mouse. Myeloid and B lineage differentiation appears normal in the bone marrow of RBP-J-inactivated mice. These results suggest that RBP-J, probably by mediating Notch signaling, controls T versus B cell fate decision in lymphoid progenitors.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin J Recombination...,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Rbpj protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Notch
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
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| pubmed:issn |
0953-8178
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
14
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
637-45
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| pubmed:dateRevised |
2009-8-12
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| pubmed:meshHeading |
pubmed-meshheading:12039915-Animals,
pubmed-meshheading:12039915-B-Lymphocytes,
pubmed-meshheading:12039915-Bone Marrow Transplantation,
pubmed-meshheading:12039915-Cell Differentiation,
pubmed-meshheading:12039915-Colony-Forming Units Assay,
pubmed-meshheading:12039915-DNA-Binding Proteins,
pubmed-meshheading:12039915-Hematopoietic Stem Cells,
pubmed-meshheading:12039915-Immunoglobulin J Recombination Signal Sequence-Binding...,
pubmed-meshheading:12039915-Lymphopoiesis,
pubmed-meshheading:12039915-Membrane Proteins,
pubmed-meshheading:12039915-Mice,
pubmed-meshheading:12039915-Mice, Inbred C57BL,
pubmed-meshheading:12039915-Mice, Knockout,
pubmed-meshheading:12039915-Mice, Transgenic,
pubmed-meshheading:12039915-Nuclear Proteins,
pubmed-meshheading:12039915-Receptors, Notch,
pubmed-meshheading:12039915-Signal Transduction,
pubmed-meshheading:12039915-T-Lymphocytes
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| pubmed:year |
2002
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| pubmed:articleTitle |
Inducible gene knockout of transcription factor recombination signal binding protein-J reveals its essential role in T versus B lineage decision.
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| pubmed:affiliation |
Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|