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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
42
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pubmed:dateCreated |
2001-10-10
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pubmed:abstractText |
We previously reported that overexpression of PU.1, a member of the Ets family of transcription factors, induces differentiation inhibition and apoptosis associated with c-Myc down-regulation in murine erythroleukemia (MEL) cells. To understand the molecular mechanism by which c-Myc is down-regulated due to overexpression of PU.1, we performed luciferase reporter assays using the mouse c-myc promoter. PU.1 repressed the activities of not only the c-myc promoter but also several other promoters. Experiments with deletion mutants of PU.1 revealed that the C-terminal region spanning amino acids (aa) 123-272 including the PEST and ETS domains but not the activation domain was sufficient for this transcriptional repression. It was unlikely that the repression was due to sequestration of a limited amount of CBP/p300 nor pCAF, because overexpression of these co-activators did not relieve PU.1-mediated transcriptional repression. Instead, it was found that the C-terminal aa 101-272 of PU.1 formed a complex with mSin3A and HDAC1 in vivo, which was speculated to be associated with the repression. The C-terminal region of PU.1 also formed a complex with the basic transcription factor TBP in vitro and in vivo. Our results suggest that overexpression of PU.1 induces transcriptional repression in several gene promoters including the c-myc promoter which may be mediated by its complex formation with HDACs.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/HDAC1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Histone Deacetylases,
http://linkedlifedata.com/resource/pubmed/chemical/Macromolecular Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-myc,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/SIN3A transcription factor,
http://linkedlifedata.com/resource/pubmed/chemical/TATA-Box Binding Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/proto-oncogene protein Spi-1
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0950-9232
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
20
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6039-47
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11593411-Cell Line,
pubmed-meshheading:11593411-DNA-Binding Proteins,
pubmed-meshheading:11593411-Down-Regulation,
pubmed-meshheading:11593411-Genes, Reporter,
pubmed-meshheading:11593411-HeLa Cells,
pubmed-meshheading:11593411-Histone Deacetylase 1,
pubmed-meshheading:11593411-Histone Deacetylases,
pubmed-meshheading:11593411-Humans,
pubmed-meshheading:11593411-Macromolecular Substances,
pubmed-meshheading:11593411-Mutation,
pubmed-meshheading:11593411-Promoter Regions, Genetic,
pubmed-meshheading:11593411-Protein Structure, Tertiary,
pubmed-meshheading:11593411-Proto-Oncogene Proteins,
pubmed-meshheading:11593411-Proto-Oncogene Proteins c-myc,
pubmed-meshheading:11593411-RNA, Messenger,
pubmed-meshheading:11593411-Repressor Proteins,
pubmed-meshheading:11593411-Simian virus 40,
pubmed-meshheading:11593411-TATA-Box Binding Protein,
pubmed-meshheading:11593411-Trans-Activators,
pubmed-meshheading:11593411-Transcription, Genetic,
pubmed-meshheading:11593411-Transcription Factors
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pubmed:year |
2001
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pubmed:articleTitle |
In vivo complex formation of PU.1 with HDAC1 associated with PU.1-mediated transcriptional repression.
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pubmed:affiliation |
Department of Cell Genetics, Sasaki Institute, 2-2, Kanda-Surugadai, Chiyoda-ku, Tokyo 101-0062, Japan.
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pubmed:publicationType |
Journal Article
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