pubmed-article:9584201 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0376622 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0205112 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0242643 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0035143 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C0162768 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C1514562 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
pubmed-article:9584201 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:9584201 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:9584201 | pubmed:dateCreated | 1998-6-17 | lld:pubmed |
pubmed-article:9584201 | pubmed:abstractText | Chromosomal translocations in acute leukemia that affect the AML-1/CBFbeta transcription factor complex create dominant inhibitory proteins. However, the mechanisms by which these proteins act remain obscure. Here we demonstrate that the multidrug resistance 1 (MDR-1) promoter is a target for AML/ETO transcriptional repression. This repression is of basal, not activated, expression from the MDR-1 promoter and thus represents a new mechanism for AML/ETO function. We have defined two domains in AML/ETO that are required for repression of basal transcription from the MDR-1 promoter: a hydrophobic heptad repeat (HHR) motif and a conserved zinc finger (ZnF) domain termed the MYND domain. The HHR mediates formation of AML/ETO homodimers and AML/ETO-ETO heterodimers. Single serine substitutions at conserved cysteine residues within the predicted ZnFs also abrogate transcriptional repression. Finally, we observe that AML/ETO can also inhibit Ets-1 activation of the MDR-1 promoter, indicating that AML/ETO can disrupt both basal and Ets-1-dependent transcription. The fortuitous inhibition of MDR-1 expression in t(8;21)-containing leukemias may contribute to the favorable response of these patients to chemotherapeutic drugs. | lld:pubmed |
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pubmed-article:9584201 | pubmed:language | eng | lld:pubmed |
pubmed-article:9584201 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9584201 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9584201 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9584201 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9584201 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9584201 | pubmed:month | Jun | lld:pubmed |
pubmed-article:9584201 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:9584201 | pubmed:author | pubmed-author:SunDD | lld:pubmed |
pubmed-article:9584201 | pubmed:author | pubmed-author:HiebertS WSW | lld:pubmed |
pubmed-article:9584201 | pubmed:author | pubmed-author:SchuetzJJ | lld:pubmed |
pubmed-article:9584201 | pubmed:author | pubmed-author:LutterbachBB | lld:pubmed |
pubmed-article:9584201 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9584201 | pubmed:volume | 18 | lld:pubmed |
pubmed-article:9584201 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9584201 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9584201 | pubmed:pagination | 3604-11 | lld:pubmed |
pubmed-article:9584201 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:9584201 | pubmed:meshHeading | pubmed-meshheading:9584201-... | lld:pubmed |