Source:http://linkedlifedata.com/resource/pubmed/id/11448937
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
14
|
| pubmed:dateCreated |
2001-7-12
|
| pubmed:abstractText |
The elements controlling the complex developmental and tissue-specific expression of the cystic fibrosis transmembrane conductance regulator (CFTR) gene lie outside the basal promoter region and have not been characterized. We previously identified a tissue-specific DNase I hypersensitive site (DHS) in intron 1 (185 + 10 kb) of the CFTR gene. Here we show that removal of the core element abolishes the activity of this DHS in transient transfection assays of reporter/enhancer gene constructs. We then compared expression from a 310 kb yeast artificial chromosome (YAC) that contains the entire CFTR gene with expression from the same YAC from which the DHS element had been deleted. Stable transfection of a human colon carcinoma cell line showed that transcription from the deleted YAC was reduced by approximately 60%. In transgenic mice, deletion of the intron 1 DHS had no effect on expression in the lung, but reduced expression in the intestine by approximately 60%. Thus, the regulatory element associated with the intron 1 DHS is tissue-specific and is required for normal CFTR expression levels in the intestinal epithelium in vivo.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CFTR protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cystic Fibrosis Transmembrane...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxyribonuclease I
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0964-6906
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
10
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1455-64
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:11448937-Animals,
pubmed-meshheading:11448937-Caco-2 Cells,
pubmed-meshheading:11448937-Cell Line,
pubmed-meshheading:11448937-Chromosomes, Artificial, Yeast,
pubmed-meshheading:11448937-Cystic Fibrosis Transmembrane Conductance Regulator,
pubmed-meshheading:11448937-DNA-Binding Proteins,
pubmed-meshheading:11448937-Deoxyribonuclease I,
pubmed-meshheading:11448937-Gene Expression Regulation,
pubmed-meshheading:11448937-Humans,
pubmed-meshheading:11448937-Intestines,
pubmed-meshheading:11448937-Introns,
pubmed-meshheading:11448937-Mice,
pubmed-meshheading:11448937-Mice, Inbred C57BL,
pubmed-meshheading:11448937-Mice, Transgenic,
pubmed-meshheading:11448937-Polymerase Chain Reaction,
pubmed-meshheading:11448937-Regulatory Sequences, Nucleic Acid,
pubmed-meshheading:11448937-Tissue Distribution,
pubmed-meshheading:11448937-Transcription, Genetic,
pubmed-meshheading:11448937-Transfection
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
An element in intron 1 of the CFTR gene augments intestinal expression in vivo.
|
| pubmed:affiliation |
Paediatric Molecular Genetics, Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|