| pubmed-article:10023670 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10023670 | lifeskim:mentions | umls-concept:C0085133 | lld:lifeskim |
| pubmed-article:10023670 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:10023670 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:10023670 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:10023670 | lifeskim:mentions | umls-concept:C1705630 | lld:lifeskim |
| pubmed-article:10023670 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:10023670 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10023670 | pubmed:dateCreated | 1999-2-23 | lld:pubmed |
| pubmed-article:10023670 | pubmed:abstractText | A common characteristic of malignant cells derived from patients with Hodgkin's disease (HD) is a high level of constitutive nuclear NF-kappaB/Rel activity, which stimulates proliferation and confers resistance to apoptosis. We have analysed the mechanisms that account for NF-kappaB activation in a panel of Hodgkin/Reed-Sternberg (H-RS) cell lines. Whereas two cell lines (L428 and KMH-2) expressed inactive IkappaBalpha, no significant changes in NF-kappaB or IkappaB expression were seen in other H-RS cells (L591, L1236 and HDLM-2). Constitutive NF-kappaB was susceptible to inhibition by recombinant IkappaBalpha, suggesting that neither mutations in the NF-kappaB genes nor posttranslational modifications of NF-kappaB were involved. Endogenous IkappaBalpha was bound to p65 and displayed a very short half-life. IkappaBalpha degradation could be blocked by inhibitors of the NF-kappaB activating pathway. Proteasomal inhibition caused an accumulation of phosphorylated IkappaBalpha and a reduction of NF-kappaB activity in HDLM-2 and L1236 cells. By in vitro kinase assays we demonstrate constitutive IkappaB kinase (IKK) activity in H-RS cells, indicating ongoing signal transduction. Furthermore, H-RS cells secrete one or more factor(s) that were able to trigger NF-kappaB activation. We conclude that aberrant activation of IKK's, and in some cases defective IkappaBs, lead to constitutive nuclear NF-kappaB activity, which in turn results in a growth advantage of Hodgkin's disease tumor cells. | lld:pubmed |
| pubmed-article:10023670 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10023670 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10023670 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10023670 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10023670 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:10023670 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:10023670 | pubmed:author | pubmed-author:DörkenBB | lld:pubmed |
| pubmed-article:10023670 | pubmed:author | pubmed-author:ScheidereitCC | lld:pubmed |
| pubmed-article:10023670 | pubmed:author | pubmed-author:EmmerichFF | lld:pubmed |
| pubmed-article:10023670 | pubmed:author | pubmed-author:KrappmannDD | lld:pubmed |
| pubmed-article:10023670 | pubmed:author | pubmed-author:KordesUU | lld:pubmed |
| pubmed-article:10023670 | pubmed:author | pubmed-author:ScharschmidtE... | lld:pubmed |
| pubmed-article:10023670 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10023670 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:10023670 | pubmed:volume | 18 | lld:pubmed |
| pubmed-article:10023670 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10023670 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10023670 | pubmed:pagination | 943-53 | lld:pubmed |
| pubmed-article:10023670 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10023670 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10023670 | pubmed:articleTitle | Molecular mechanisms of constitutive NF-kappaB/Rel activation in Hodgkin/Reed-Sternberg cells. | lld:pubmed |
| pubmed-article:10023670 | pubmed:affiliation | Max-Delbrück-Centrum for Molecular Medicine, Berlin, Germany. | lld:pubmed |
| pubmed-article:10023670 | pubmed:publicationType | Journal Article | lld:pubmed |
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