| pubmed-article:12060665 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0439849 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0126732 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0031715 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0077503 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0033681 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C1334877 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C1512167 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12060665 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:12060665 | pubmed:issue | 34 | lld:pubmed |
| pubmed-article:12060665 | pubmed:dateCreated | 2002-8-19 | lld:pubmed |
| pubmed-article:12060665 | pubmed:abstractText | Bcr-Abl, the product of the protooncogene bcr-abl, is a constitutively active protein-tyrosine kinase that is highly expressed in chronic myelogenous leukemia and in acute myeloid leukemia cells. Because Bcr-Abl is known to provide mitogenic signals through suppression of apoptosis, we investigated the effect of this oncogene product on signaling by tumor necrosis factor (TNF), a proapoptotic cytokine. We used a bcr-abl-deficient human megakaryocytic leukemia cell line MO7E and an isogenic MBA cell line stably transfected with bcr-abl. Electrophoretic mobility shift assay revealed that TNF activated the nuclear transcription factor NF-kappaB in MO7E cells but not in MBA cells. The impaired NF-kappaB activation in Bcr-Abl-expressing cells was not due to absence of the NF-kappaB proteins p65, p50, or p100 or of IkappaBalpha or IkappaBbeta. Okadaic acid-induced NF-kappaB activation was unaffected by Bcr-Abl expression. TNF induced IkappaBalpha phosphorylation and degradation in MO7E cells but not in MBA cells. The suppression of TNF-induced NF-kappaB activation by Bcr-Abl was not restricted to MBA cells, because ectopic expression of Bcr-Abl in human acute myeloid leukemia HL-60 cells also blocked TNF-induced NF-kappaB activation. When examined for the TNF receptors by the radioreceptor assay, flow cytometry, or Western blot analysis, we found that Bcr-Abl expression down-regulated the expression of the TNF receptors. The RNase protection assay and Northern blot analysis revealed the transcriptional down-regulation of the TNF receptor by Bcr-Abl protein. Overall, these results indicate that ectopic expression of Bcr-Abl interferes with the TNF signaling pathway through the down-regulation of TNF receptors. | lld:pubmed |
| pubmed-article:12060665 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12060665 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12060665 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12060665 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:12060665 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:MukhopadhyayA... | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:AggarwalBhara... | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:BhallaKapil... | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:ShishodiaShis... | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:LamotheBettyB | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:SuttlesJillJ | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:BrittinghamKa... | lld:pubmed |
| pubmed-article:12060665 | pubmed:author | pubmed-author:NimmanapalliR... | lld:pubmed |
| pubmed-article:12060665 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12060665 | pubmed:day | 23 | lld:pubmed |
| pubmed-article:12060665 | pubmed:volume | 277 | lld:pubmed |
| pubmed-article:12060665 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12060665 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12060665 | pubmed:pagination | 30622-8 | lld:pubmed |
| pubmed-article:12060665 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
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| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
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| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:meshHeading | pubmed-meshheading:12060665... | lld:pubmed |
| pubmed-article:12060665 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12060665 | pubmed:articleTitle | Ectopic expression of protein-tyrosine kinase Bcr-Abl suppresses tumor necrosis factor (TNF)-induced NF-kappa B activation and IkappaBalpha phosphorylation. Relationship with down-regulation of TNF receptors. | lld:pubmed |
| pubmed-article:12060665 | pubmed:affiliation | Cytokine Research Laboratory, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. | lld:pubmed |
| pubmed-article:12060665 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12060665 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
