Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:12481899rdf:typepubmed:Citationlld:pubmed
pubmed-article:12481899lifeskim:mentionsumls-concept:C0007634lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0012655lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0023434lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0162638lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0079925lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0085862lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0376515lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C1299583lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C0392756lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C1608386lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C1549571lld:lifeskim
pubmed-article:12481899lifeskim:mentionsumls-concept:C1519595lld:lifeskim
pubmed-article:12481899pubmed:issue10lld:pubmed
pubmed-article:12481899pubmed:dateCreated2002-12-16lld:pubmed
pubmed-article:12481899pubmed:abstractTextOur previous work demonstrated that antisense oligonucleotides complementary to Bcl-2 mRNA sequences were able to reduce Bcl-2 protein expression in B-cell chronic lymphocytic leukaemia (B-CLL) cells. Furthermore, the reduction in Bcl-2 expression led to an increase in apoptotic cell death that was associated with an increase in Bax expression. In this present study antisense oligonucleotides directed towards the Bax translation initiation sequence were employed to determine whether Bcl-2 and Bax protein expression were interdependent upon one another and whether Bcl-2 antisense-induced apoptosis was mediated through a p53-dependent cell death pathway. The antisense oligonucleotide down-regulated Bax protein expression between 23.7 and 68.8% in the 20 B-CLL samples tested and significantly inhibited apoptotic cell death when compared to controls (p = 0.0001). Furthermore, these changes were independent of Bcl-2 expression suggesting that the previously observed increase in Bax expression following exposure of B-CLL cells to Bcl-2 antisense oligonucleotides was probably caused by the induction of apoptosis rather than a rheostatic response to the reduction in Bcl-2 protein expression. This notion was substantiated by the fact that p21 expression was induced in Bcl-2 antisense-treated B-CLL cells, a finding consistent with p53 activation.lld:pubmed
pubmed-article:12481899pubmed:languageenglld:pubmed
pubmed-article:12481899pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:citationSubsetIMlld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12481899pubmed:statusMEDLINElld:pubmed
pubmed-article:12481899pubmed:monthOctlld:pubmed
pubmed-article:12481899pubmed:issn1042-8194lld:pubmed
pubmed-article:12481899pubmed:authorpubmed-author:ThomasAlunAlld:pubmed
pubmed-article:12481899pubmed:authorpubmed-author:HoyTerryTlld:pubmed
pubmed-article:12481899pubmed:authorpubmed-author:PepperChrisClld:pubmed
pubmed-article:12481899pubmed:authorpubmed-author:BentleyPaulPlld:pubmed
pubmed-article:12481899pubmed:issnTypePrintlld:pubmed
pubmed-article:12481899pubmed:volume43lld:pubmed
pubmed-article:12481899pubmed:ownerNLMlld:pubmed
pubmed-article:12481899pubmed:authorsCompleteYlld:pubmed
pubmed-article:12481899pubmed:pagination2003-9lld:pubmed
pubmed-article:12481899pubmed:dateRevised2007-11-15lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:meshHeadingpubmed-meshheading:12481899...lld:pubmed
pubmed-article:12481899pubmed:year2002lld:pubmed
pubmed-article:12481899pubmed:articleTitleAntisense oligonucleotides complementary to Bax transcripts reduce the susceptibility of B-cell chronic lymphocytic leukaemia cells to apoptosis in a bcl-2 independent manner.lld:pubmed
pubmed-article:12481899pubmed:affiliationDepartment of Haematology, Llandough Hospital, Penlan Road, Penarth, Vale of Glamorgan, CF64 2XX, UK. chrisp@llanhaem.demon.co.uklld:pubmed
pubmed-article:12481899pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12481899pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
entrez-gene:581entrezgene:pubmedpubmed-article:12481899lld:entrezgene
entrez-gene:596entrezgene:pubmedpubmed-article:12481899lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:12481899lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:12481899lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12481899lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12481899lld:pubmed