rdf:type |
|
lifeskim:mentions |
umls-concept:C0012591,
umls-concept:C0024662,
umls-concept:C0040649,
umls-concept:C0086860,
umls-concept:C0205145,
umls-concept:C0205160,
umls-concept:C0439659,
umls-concept:C0851285,
umls-concept:C1158770,
umls-concept:C1333247,
umls-concept:C1417833,
umls-concept:C1446409,
umls-concept:C1519249,
umls-concept:C1554184
|
pubmed:issue |
10
|
pubmed:dateCreated |
1995-6-16
|
pubmed:abstractText |
Ear3/COUP is an orphan member of the steroid/thyroid hormone receptor superfamily of transcription factors and binds most tightly to a direct repeat of AGGTCA with 1 nucleotide in between (DR1). Ear3/COUP also binds with a similar affinity to the palindromic thyroid hormone response element (TRE). This binding preference of Ear3/COUP is same as that of the retinoid X receptor (RXR), which is another member of the superfamily. In the present study, we identified a sequence responsible for Ear3/COUP-mediated transactivation in the region downstream of the transcription start site of the mouse mammary tumor virus promoter. This cis-acting sequence was unresponsive to RXR. When the DR1 or TRE sequence was added upstream of the promoter, transactivation by Ear3/COUP was completely abolished, whereas RXR enhanced transcription from the promoter. The mode of action of Ear3/COUP could be utilized to control complex gene expressions in morphogenesis, homeostasis, and development.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1311101,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1312668,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1324415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1327536,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1438252,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1517211,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1550558,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1648450,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1662118,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-1671296,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2047861,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2105166,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2159111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2500251,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2644044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2726731,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2739739,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2848197,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-2853466,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3037497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3040258,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3191531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3283939,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3396073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3670376,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7753823-3909942
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
May
|
pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
9
|
pubmed:volume |
92
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
4432-6
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:7753823-Animals,
pubmed-meshheading:7753823-Base Sequence,
pubmed-meshheading:7753823-Binding Sites,
pubmed-meshheading:7753823-COUP Transcription Factor I,
pubmed-meshheading:7753823-Chloramphenicol O-Acetyltransferase,
pubmed-meshheading:7753823-DNA-Binding Proteins,
pubmed-meshheading:7753823-Gene Expression Regulation,
pubmed-meshheading:7753823-Mammary Tumor Virus, Mouse,
pubmed-meshheading:7753823-Molecular Sequence Data,
pubmed-meshheading:7753823-Mutagenesis,
pubmed-meshheading:7753823-Oligodeoxyribonucleotides,
pubmed-meshheading:7753823-Promoter Regions, Genetic,
pubmed-meshheading:7753823-Receptors, Retinoic Acid,
pubmed-meshheading:7753823-Repetitive Sequences, Nucleic Acid,
pubmed-meshheading:7753823-Restriction Mapping,
pubmed-meshheading:7753823-Retinoid X Receptors,
pubmed-meshheading:7753823-Sequence Deletion,
pubmed-meshheading:7753823-TATA Box,
pubmed-meshheading:7753823-Thymidine Kinase,
pubmed-meshheading:7753823-Transcription, Genetic,
pubmed-meshheading:7753823-Transcription Factors,
pubmed-meshheading:7753823-Transcriptional Activation,
pubmed-meshheading:7753823-Transfection
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pubmed:year |
1995
|
pubmed:articleTitle |
Dual transcriptional control by Ear3/COUP: negative regulation through the DR1 direct repeat and positive regulation through a sequence downstream of the transcriptional start site of the mouse mammary tumor virus promoter.
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pubmed:affiliation |
Department of Oncology, University of Tokyo, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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