Source:http://linkedlifedata.com/resource/pubmed/id/16247445
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2006-3-2
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pubmed:abstractText |
A 117 bp fragment of the human ELA2 promoter has been characterized that can act as a minimal promoter for the expression of neutrophil elastase. Chromatin immunoprecipitation and siRNAs revealed that expression of ELA2 is regulated by the acute myeloid human leukemia 1 protein (AML1), C/EBPalpha, PU.1 and c-Myb transcription factors. ELA2 has also been investigated as a possible target of the leukemic fusion protein AML1-ETO resulting from the t(8;21) chromosomal translocation. AML1-ETO, like AML1, binds the ELA2 promoter in the myeloid cell lines Kasumi-1 and U937, but unexpectedly fails to significantly alter expression of ELA2. Although AML1-ETO downregulates the expression of C/EBPalpha, changes in C/EBPalpha expression do not correlate with changes in the expression of ELA2. Our observations indicate that AML1-ETO may not be a constitutive repressor of gene expression in every case in which it can associate with DNA, either on its own or in conjunction with C/EBPalpha. Since neither ETO nor AML1-ETO are typically expressed in hematopoietic progenitors, we hypothesize that it is the interactions between AML1-ETO and regulatory cofactors in disease-state cells that alter gene expression programs during hematopoiesis. These protein-protein interactions may not require simultaneous DNA binding by AML1-ETO for the deleterious effects of the fusion protein to be realized.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AML1-ETO fusion protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Core Binding Factor Alpha 2 Subunit,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Oncogene Proteins, Fusion,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/pancreatic elastase II
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
2
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1349-57
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:16247445-Acute Disease,
pubmed-meshheading:16247445-Chromatin Immunoprecipitation,
pubmed-meshheading:16247445-Core Binding Factor Alpha 2 Subunit,
pubmed-meshheading:16247445-DNA-Binding Proteins,
pubmed-meshheading:16247445-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16247445-Hematopoiesis,
pubmed-meshheading:16247445-Humans,
pubmed-meshheading:16247445-Leukemia, Myeloid,
pubmed-meshheading:16247445-Oncogene Proteins, Fusion,
pubmed-meshheading:16247445-Promoter Regions, Genetic,
pubmed-meshheading:16247445-RNA, Small Interfering,
pubmed-meshheading:16247445-Serine Endopeptidases,
pubmed-meshheading:16247445-Transcription Factors
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pubmed:year |
2006
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pubmed:articleTitle |
ELA2 is regulated by hematopoietic transcription factors, but not repressed by AML1-ETO.
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pubmed:affiliation |
Laboratory of Molecular Biophysics, The Rockefeller University, New York, NY 10021, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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