Linked Life Data

12732181

Source:http://linkedlifedata.com/resource/pubmed/id/12732181

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-5-6
pubmed:abstractText
The t(8;21) is one of the most frequent chromosomal translocations associated with acute leukemia. The translocation fuses the DNA binding domain of AML1 to nearly all of the ETO co-repressor. ETO associates with the mSin3 and N-CoR co-repressors as well as histone deacetylases 1, 2, and 3. Although this is one of the most frequent chromosomal translocations in acute leukemia, accounting for 10-15% of the cases of acute myeloid leukemia (AML), the direct targets for transcriptional regulation that stimulate leukemogenesis are unknown. We found that AML1-ETO repressed the promoter of p14(ARF) tumor suppressor in transient transfection assays and reduced endogenous levels of p14(ARF) expression in multiple cell types. Chromatin immunoprecipitation assays demonstrated that AML1-ETO bound to the p14(ARF) promoter. In acute myeloid leukemia samples containing the t(8;21), levels of p14(ARF) mRNA were markedly lower when compared to other acute myeloid leukemias. Therefore, p14(ARF) is a direct transcriptional target of AML1-ETO.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1079-9796
pubmed:author
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-83
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:articleTitle
The t(8;21) fusion protein contacts co-repressors and histone deacetylases to repress the transcription of the p14ARF tumor suppressor.
pubmed:affiliation
Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. scott.hiebert@mcmai.vanderbilt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't