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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2009-1-8
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pubmed:abstractText |
Fas-associated protein with death domain/mediator of receptor induced toxicity (FADD/MORT1) was first described as a transducer of death receptor signalling but was later recognized also to be important for proliferation of T cells. B-cell lymphoma 3 (Bcl-3) is a relatively little understood member of the nuclear factor (NF)-kappaB family of transcription factors. We recently found that Bcl-3 is up-regulated in T cells from mice where FADD function is blocked by a dominant negative transgene (FADD-DN). To understand the importance of this, we generated FADD-DN/bcl-3(-/-) mice. Here, we report that T cells from these mice show massive cell death and severely reduced proliferation in response to T-cell receptor (TCR) stimulation in vitro. Transgenic co-expression of Bcl-2 (FADD-DN/bcl-3(-/-)/vav-bcl-2 mice) rescued the survival but not the proliferation of T cells. FADD-DN/bcl-3(-/-) mice had normal thymocyte numbers but reduced numbers of peripheral T cells despite an increase in cycling T cells in vivo. However, activation of the classical NF-kappaB and extracellular regulated kinase (ERK) pathways and expression of interleukin (IL)-2 mRNA upon stimulation were normal in T cells from FADD-DN/bcl-3(-/-) mice. These data suggest that FADD and Bcl-3 regulate separate pathways that both contribute to survival and proliferation in mouse T cells.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-10611317,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-10894163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-11250157,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-11323692,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-11713278,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-11950875,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-12055593,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-12110583,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-12115619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-12215447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-12353035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-12654726,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-15322156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-15376191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-15479861,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-15905188,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-16043517,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-16043518,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-16123212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-16709845,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-16832056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-17332376,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-17585338,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9133427,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9450996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9506948,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9521326,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9586634,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9721089,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18557791-9729047
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1365-2567
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
125
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
549-57
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pubmed:dateRevised |
2010-9-21
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pubmed:meshHeading |
pubmed-meshheading:18557791-Animals,
pubmed-meshheading:18557791-Cell Proliferation,
pubmed-meshheading:18557791-Cell Survival,
pubmed-meshheading:18557791-Fas-Associated Death Domain Protein,
pubmed-meshheading:18557791-MAP Kinase Signaling System,
pubmed-meshheading:18557791-Mice,
pubmed-meshheading:18557791-Mice, Inbred C57BL,
pubmed-meshheading:18557791-Mice, Knockout,
pubmed-meshheading:18557791-Mice, Transgenic,
pubmed-meshheading:18557791-NF-kappa B,
pubmed-meshheading:18557791-Proto-Oncogene Proteins,
pubmed-meshheading:18557791-Receptors, Antigen, T-Cell,
pubmed-meshheading:18557791-Signal Transduction,
pubmed-meshheading:18557791-T-Lymphocytes,
pubmed-meshheading:18557791-Transcription Factors
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pubmed:year |
2008
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pubmed:articleTitle |
FADD and the NF-kappaB family member Bcl-3 regulate complementary pathways to control T-cell survival and proliferation.
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pubmed:affiliation |
Institute for Medical Microbiology, Technische Universität München, Munich, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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