Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-2-3
pubmed:abstractText
The murine Htf9-a/RanBP1 and Htf9-c genes are divergently transcribed from a shared TATA-less promoter. Transcription of both genes is initiated on complementary DNA strands and is controlled by cell cycle-dependent mechanisms. The bidirectional promoter harbors a genomic footprint flanking the major transcription start site of both genes. Transient promoter assays showed that the footprinted element is important for transcription of both genes. Protein-binding experiments and antibody assays indicated that members of the retinoid X receptor family interact with the double-stranded site. In addition, distinct factors interact with single DNA strands of the element. Double-stranded binding factors were highly expressed in liver cells, in which neither gene is transcribed, while single-stranded binding proteins were abundant in cycling cells, in which transcription of both genes is efficient. In vivo S1 analysis of the promoter depicted an S1-sensitive organization in cells in which transcription of both genes is active; S1 sensitivity was not detected in conditions of transcriptional repression. Thus, the same element is a target for either retinoid X receptor factors, or for single-stranded binding proteins, and form distinct complexes in different cellular conditions depending on the DNA conformation in the binding site.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cell Extracts, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Single-Stranded, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Htf9c protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Retinoic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Retinoid X Receptors, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/ran GTP-Binding Protein, http://linkedlifedata.com/resource/pubmed/chemical/ran-binding protein 1
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
273
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
495-505
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9417108-3T3 Cells, pubmed-meshheading:9417108-Animals, pubmed-meshheading:9417108-Base Sequence, pubmed-meshheading:9417108-Binding Sites, pubmed-meshheading:9417108-Cell Extracts, pubmed-meshheading:9417108-DNA, Single-Stranded, pubmed-meshheading:9417108-DNA Footprinting, pubmed-meshheading:9417108-DNA-Binding Proteins, pubmed-meshheading:9417108-Fibroblasts, pubmed-meshheading:9417108-GTP-Binding Proteins, pubmed-meshheading:9417108-Liver, pubmed-meshheading:9417108-Mice, pubmed-meshheading:9417108-Molecular Sequence Data, pubmed-meshheading:9417108-Mutation, pubmed-meshheading:9417108-Nuclear Proteins, pubmed-meshheading:9417108-Promoter Regions, Genetic, pubmed-meshheading:9417108-Proteins, pubmed-meshheading:9417108-Receptors, Retinoic Acid, pubmed-meshheading:9417108-Retinoid X Receptors, pubmed-meshheading:9417108-Transcription Factors, pubmed-meshheading:9417108-Transcriptional Activation, pubmed-meshheading:9417108-ran GTP-Binding Protein
pubmed:year
1998
pubmed:articleTitle
Interactions with single-stranded and double-stranded DNA-binding factors and alternative promoter conformation upon transcriptional activation of the Htf9-a/RanBP1 and Htf9-c genes.
pubmed:affiliation
CNR Centre of Evolutionary Genetics, c/o Department of Genetics and Molecular Biology, University "La Sapienza," Rome 00185, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't