pubmed-article:11046018 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C0040648 | lld:lifeskim |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
pubmed-article:11046018 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:11046018 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:11046018 | pubmed:dateCreated | 2000-11-3 | lld:pubmed |
pubmed-article:11046018 | pubmed:abstractText | We and others have reported that IFN-alpha potentiates the apoptotic effects of TNF through a mechanism that is not understood. Because the nuclear transcription factors NF-kappaB and AP-1 have recently been reported to mediate anti-apoptosis and cell survival, we hypothesized that IFN-alpha potentiates the cytotoxic effects of TNF by suppressing TNF-induced activation of NF-kappaB and AP-1. We tested this hypothesis by pretreating human Jurkat T cells with IFN-alpha, which blocked TNF-induced activation of NF-kappaB and AP-1 in a time- and dose-dependent manner as determined by EMSA. IFN-alpha blocked TNF-induced phosphorylation and degradation of the inhibitor subunit of NF-kappaB, and suppressed NF-kappaB and AP-1 activation induced by various other inflammatory stimuli. NF-kappaB-dependent reporter gene expression activated by TNF, TNFR1, TNF receptor-associated factor 2, and NF-kappaB-inducing kinase was also abrogated by IFN-alpha pretreatment. The suppression of NF-kappaB and AP-1 correlated with the potentiation of TNF-induced cytotoxicity and caspase activation. Overall our results suggest that IFN-alpha potentiates the apoptotic effects of TNF possibly by suppressing NF-kappaB and AP-1 activation. | lld:pubmed |
pubmed-article:11046018 | pubmed:language | eng | lld:pubmed |
pubmed-article:11046018 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11046018 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11046018 | pubmed:month | Nov | lld:pubmed |
pubmed-article:11046018 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:11046018 | pubmed:author | pubmed-author:AggarwalB BBB | lld:pubmed |
pubmed-article:11046018 | pubmed:author | pubmed-author:MukhopadhyayA... | lld:pubmed |
pubmed-article:11046018 | pubmed:author | pubmed-author:MannaS KSK | lld:pubmed |
pubmed-article:11046018 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11046018 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11046018 | pubmed:volume | 165 | lld:pubmed |
pubmed-article:11046018 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11046018 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11046018 | pubmed:pagination | 4927-34 | lld:pubmed |
pubmed-article:11046018 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:11046018 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:11046018 | pubmed:articleTitle | IFN-alpha suppresses activation of nuclear transcription factors NF-kappa B and activator protein 1 and potentiates TNF-induced apoptosis. | lld:pubmed |
pubmed-article:11046018 | pubmed:affiliation | Cytokine Research Laboratory, Department of Bioimmunotherapy, MD Anderson Cancer Center, University of Texas, Houston, TX 77030, USA. | lld:pubmed |
pubmed-article:11046018 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11046018 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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