| pubmed-article:11034214 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C1506928 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C1705438 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C0812244 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C1515144 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:11034214 | lifeskim:mentions | umls-concept:C0205214 | lld:lifeskim |
| pubmed-article:11034214 | pubmed:issue | 6804 | lld:pubmed |
| pubmed-article:11034214 | pubmed:dateCreated | 2000-10-19 | lld:pubmed |
| pubmed-article:11034214 | pubmed:abstractText | Strong stimulation of the T-cell receptor (TCR) on cycling peripheral T cells causes their apoptosis by a process called TCR-activation-induced cell death (TCR-AICD). TCR-AICD occurs from a late G1 phase cell-cycle check point independently of the 'tumour suppressor' protein p53. Disruption of the gene for the E2F-1 transcription factor, an inducer of apoptosis, causes significant increases in T-cell number and splenomegaly. Here we show that T cells undergoing TCR-AICD induce the p53-related gene p73, another mediator of apoptosis, which is hypermethylated in lymphomas. Introducing a dominant-negative E2F-1 protein or a dominant-negative p73 protein into T cells protects them from TCR-mediated apoptosis, whereas dominant-negative E2F-2, E2F-4 or p53 does not. Furthermore, E2F-1-null or p73-null primary T cells do not undergo TCR-mediated apoptosis either. We conclude that TCR-AICD occurs from a late G1 cell-cycle checkpoint that is dependent on both E2F-1 and p73 activities. These observations indicate that, unlike p53, p73 serves to integrate receptor-mediated apoptotic stimuli. | lld:pubmed |
| pubmed-article:11034214 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11034214 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11034214 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11034214 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11034214 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11034214 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:11034214 | pubmed:issn | 0028-0836 | lld:pubmed |
| pubmed-article:11034214 | pubmed:author | pubmed-author:IrwinMM | lld:pubmed |
| pubmed-article:11034214 | pubmed:author | pubmed-author:DowdyS FSF | lld:pubmed |
| pubmed-article:11034214 | pubmed:author | pubmed-author:DavisP KPK | lld:pubmed |
| pubmed-article:11034214 | pubmed:author | pubmed-author:KaelinW GWG | lld:pubmed |
| pubmed-article:11034214 | pubmed:author | pubmed-author:LissyN ANA | lld:pubmed |
| pubmed-article:11034214 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11034214 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:11034214 | pubmed:volume | 407 | lld:pubmed |
| pubmed-article:11034214 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11034214 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11034214 | pubmed:pagination | 642-5 | lld:pubmed |
| pubmed-article:11034214 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11034214 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11034214 | pubmed:articleTitle | A common E2F-1 and p73 pathway mediates cell death induced by TCR activation. | lld:pubmed |
| pubmed-article:11034214 | pubmed:affiliation | Howard Hughes Medical Institute, Department of Pathology, Washington University School of Medicine, St Louis Missouri 63110, USA. | lld:pubmed |
| pubmed-article:11034214 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11034214 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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