pubmed-article:10993919 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C0205252 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C0011065 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C0814999 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C1511667 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C0332325 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C1511695 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:10993919 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:10993919 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:10993919 | pubmed:dateCreated | 2000-10-30 | lld:pubmed |
pubmed-article:10993919 | pubmed:abstractText | Immature CD4(+)CD8(+) thymocytes rearrange their T cell receptor (TCR)-alpha gene locus to generate clonotypic alpha/beta TCR, after which a few cells expressing selectable TCR are signaled to further differentiate into mature T cells. Because of requirements for self-tolerance, immature CD4(+)CD8(+) thymocytes are programmed to die in the thymus in response to a variety of stimuli that do not induce death of mature T cells. We now demonstrate that, in contrast to all previously described stimuli, immature CD4(+)CD8(+) thymocytes are selectively more resistant than mature T cells to apoptotic death induced by DNA intercalating agents. Importantly, we demonstrate that DNA intercalating agents induce double-stranded DNA breaks in both immature thymocytes and mature T cells, but immature thymocytes tolerate these DNA breaks, whereas mature T cells are signaled to die by an Atm-dependent but p53-independent death mechanism. Thus, our results indicate that absence of an Atm-dependent but p53-independent pathway allows immature thymocytes to survive double-stranded DNA breaks. It is likely that the unique ability of immature thymocytes to survive DNA-damaging intercalating agents reflects their tolerance of double-stranded DNA breaks that occur normally during antigen receptor gene rearrangements. | lld:pubmed |
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pubmed-article:10993919 | pubmed:language | eng | lld:pubmed |
pubmed-article:10993919 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10993919 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10993919 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10993919 | pubmed:month | Sep | lld:pubmed |
pubmed-article:10993919 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:10993919 | pubmed:author | pubmed-author:SingerAA | lld:pubmed |
pubmed-article:10993919 | pubmed:author | pubmed-author:BhandoolaAA | lld:pubmed |
pubmed-article:10993919 | pubmed:author | pubmed-author:NussenzweigAA | lld:pubmed |
pubmed-article:10993919 | pubmed:author | pubmed-author:DolnickBB | lld:pubmed |
pubmed-article:10993919 | pubmed:author | pubmed-author:FayadNN | lld:pubmed |
pubmed-article:10993919 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10993919 | pubmed:day | 18 | lld:pubmed |
pubmed-article:10993919 | pubmed:volume | 192 | lld:pubmed |
pubmed-article:10993919 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10993919 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10993919 | pubmed:pagination | 891-7 | lld:pubmed |
pubmed-article:10993919 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:10993919 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10993919 | pubmed:articleTitle | Immature thymocytes undergoing receptor rearrangements are resistant to an Atm-dependent death pathway activated in mature T cells by double-stranded DNA breaks. | lld:pubmed |
pubmed-article:10993919 | pubmed:affiliation | Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. bhandooa@exchange.nih.gov | lld:pubmed |
pubmed-article:10993919 | pubmed:publicationType | Journal Article | lld:pubmed |
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