pubmed-article:18557791 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C0086282 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C1333530 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:18557791 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
pubmed-article:18557791 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:18557791 | pubmed:dateCreated | 2009-1-8 | lld:pubmed |
pubmed-article:18557791 | 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. | lld:pubmed |
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pubmed-article:18557791 | pubmed:language | eng | lld:pubmed |
pubmed-article:18557791 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18557791 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18557791 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18557791 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:18557791 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18557791 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18557791 | pubmed:month | Dec | lld:pubmed |
pubmed-article:18557791 | pubmed:issn | 1365-2567 | lld:pubmed |
pubmed-article:18557791 | pubmed:author | pubmed-author:HäckerGeorgG | lld:pubmed |
pubmed-article:18557791 | pubmed:author | pubmed-author:StrasserAndre... | lld:pubmed |
pubmed-article:18557791 | pubmed:author | pubmed-author:KirschnekSusa... | lld:pubmed |
pubmed-article:18557791 | pubmed:author | pubmed-author:RangelovaSvet... | lld:pubmed |
pubmed-article:18557791 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18557791 | pubmed:volume | 125 | lld:pubmed |
pubmed-article:18557791 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18557791 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18557791 | pubmed:pagination | 549-57 | lld:pubmed |
pubmed-article:18557791 | pubmed:dateRevised | 2010-9-21 | lld:pubmed |
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pubmed-article:18557791 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18557791 | pubmed:articleTitle | FADD and the NF-kappaB family member Bcl-3 regulate complementary pathways to control T-cell survival and proliferation. | lld:pubmed |
pubmed-article:18557791 | pubmed:affiliation | Institute for Medical Microbiology, Technische Universität München, Munich, Germany. | lld:pubmed |
pubmed-article:18557791 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18557791 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:18557791 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:18557791 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:12051 | entrezgene:pubmed | pubmed-article:18557791 | lld:entrezgene |
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