Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-7-31
pubmed:abstractText
The human TR4 orphan receptor (TR4) is a member of the nuclear receptor superfamily. It functions as a transcriptional factor which regulates and controls many important physiological functions. It has been documented that TR4 may bind as a homodimer to a DNA response element containing two direct repeats of the AGGTCA consensus motif. Surprisingly, our data reveal that the expression of the human steroid 21-hydroxylase (21-OHase) gene could be repressed by TR4 via the monomeric AGGTCA motif (-228TR4RE) at its 5' flanking region (nucleotide numbers 1431-1444, 5'-GGAAAAAGGTCAGG-3'). Electrophoretic mobility shift assay showed specific binding with a dissociation constant of 0.4 nM between TR4 and the monomeric -288TR4RE motif. However, TR4 does not form heterodimers with either retinoid X receptor alpha or SHP (short heterodimer partner) orphan receptor. Additionally, both dual-luciferase and chloramphenicol acetyltransferase assays demonstrated that TR4 can function as a repressor via the -228TR4RE of the 21-OHase gene. In conclusion, our data suggest that TR4 may bind to a monomeric DNA response element and play an important role in the suppression of the 21-OHase gene expression.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
285
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1361-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
TR4 orphan receptor represses the human steroid 21-hydroxylase gene expression through the monomeric AGGTCA motif.
pubmed:affiliation
Institute of Biotechnology, National Dong Hwa University, Hualien, Taiwan, 974, Republic of China. hjlee@mail.ndhu.edu.tw
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't