| pubmed-article:11447169 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C0086661 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C1332717 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C1706438 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C0085358 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C0014372 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C1148798 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:11447169 | lifeskim:mentions | umls-concept:C1711351 | lld:lifeskim |
| pubmed-article:11447169 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:11447169 | pubmed:dateCreated | 2001-7-11 | lld:pubmed |
| pubmed-article:11447169 | pubmed:abstractText | Heat-labile enterotoxin from enterotoxinogenic Escherichia coli is not only an important cause of diarrhea in humans and domestic animals but also possesses potent immunomodulatory properties. Recently, the nontoxic, receptor-binding B subunit of heat-labile enterotoxin (EtxB) was found to induce the selective death of CD8(+) T cells, suggesting that EtxB may trigger activation of proapoptotic signaling pathways. Here we show that EtxB treatment of CD8(+) T cells but not of CD4(+) T cells triggers the specific up-regulation of the transcription factor c-myc, implicated in the control of cell proliferation, differentiation, and death. A concomitant elevation in Myc protein levels was also evident, with peak expression occurring 4 h posttreatment. Preincubation with c-myc antisense oligodeoxynucleotides demonstrated that Myc expression was necessary for EtxB-mediated apoptosis. Myc activation was also associated with an increase of IkappaBalpha turnover, suggesting that elevated Myc expression may be dependent on NF-kappaB. When CD8(+) T cells were pretreated with inhibitors of IkappaBalpha turnover and NF-kappaB translocation, this resulted in a marked reduction in both EtxB-induced apoptosis and Myc expression. Further, a non-receptor-binding mutant of EtxB, EtxB(G33D), was shown to lack the capacity to activate Myc transcription. These findings provide further evidence that EtxB is a signaling molecule that triggers activation of transcription factors involved in cell survival. | lld:pubmed |
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| pubmed-article:11447169 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11447169 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11447169 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11447169 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:11447169 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11447169 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:11447169 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:11447169 | pubmed:author | pubmed-author:WilliamsN ANA | lld:pubmed |
| pubmed-article:11447169 | pubmed:author | pubmed-author:SorianiMM | lld:pubmed |
| pubmed-article:11447169 | pubmed:author | pubmed-author:HirstT RTR | lld:pubmed |
| pubmed-article:11447169 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11447169 | pubmed:volume | 69 | lld:pubmed |
| pubmed-article:11447169 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11447169 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11447169 | pubmed:pagination | 4923-30 | lld:pubmed |
| pubmed-article:11447169 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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