pubmed-article:17952603 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0020094 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C1882071 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0285558 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C1705328 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C1705341 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0538927 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0812228 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:17952603 | lifeskim:mentions | umls-concept:C1516044 | lld:lifeskim |
pubmed-article:17952603 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:17952603 | pubmed:dateCreated | 2008-1-14 | lld:pubmed |
pubmed-article:17952603 | pubmed:abstractText | Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoproliferative disease of very poor clinical prognosis associated with infection by the human T-cell leukemia virus type I (HTLV-I). Treatment of patients with ATLL using conventional chemotherapy has limited benefit because HTLV-I cells are refractory to most apoptosis-inducing agents. In this study, we report that Celecoxib induces cell death via the intrinsic mitochondrial pathway in HTLV-I transformed leukemia cells. Treatment with Celecoxib was associated with activation of Bax, decreased expression of Mcl-1, loss of the mitochondrial membrane potential and caspase-9-dependent apoptosis. These effects were independent from Bcl-2 and Bcl-xL. We also found that Celecoxib inhibited the Akt/GSK3 beta survival pathway in HTLV-I cells. | lld:pubmed |
pubmed-article:17952603 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:language | eng | lld:pubmed |
pubmed-article:17952603 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17952603 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17952603 | pubmed:month | Jan | lld:pubmed |
pubmed-article:17952603 | pubmed:issn | 1360-8185 | lld:pubmed |
pubmed-article:17952603 | pubmed:author | pubmed-author:TaylorJohn... | lld:pubmed |
pubmed-article:17952603 | pubmed:author | pubmed-author:NicotChristop... | lld:pubmed |
pubmed-article:17952603 | pubmed:author | pubmed-author:BrownMeganM | lld:pubmed |
pubmed-article:17952603 | pubmed:author | pubmed-author:Sinha-DattaUm... | lld:pubmed |
pubmed-article:17952603 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17952603 | pubmed:volume | 13 | lld:pubmed |
pubmed-article:17952603 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17952603 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17952603 | pubmed:pagination | 33-40 | lld:pubmed |
pubmed-article:17952603 | pubmed:dateRevised | 2010-9-17 | lld:pubmed |
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pubmed-article:17952603 | pubmed:meshHeading | pubmed-meshheading:17952603... | lld:pubmed |
pubmed-article:17952603 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:17952603 | pubmed:articleTitle | Celecoxib disrupts the canonical apoptotic network in HTLV-I cells through activation of Bax and inhibition of PKB/Akt. | lld:pubmed |
pubmed-article:17952603 | pubmed:affiliation | Department of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, KS 66160, USA. | lld:pubmed |
pubmed-article:17952603 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17952603 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17952603 | lld:pubmed |