Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
1993-4-23
|
pubmed:abstractText |
A combination of linker scanning mutagenesis and deletional analyses has been used to determine the role of individual DNA-protein binding sites on expression from the hepatitis B virus (HBV) enhancer I-X promoter (map position (mp) 1042-1354, HBV adw2). Linker scanning mutation of the EF-C site caused a 67.5% drop in X promoter activity in HuH7 cells, but had no effect in HepG2 or HepSK cells. Mutation of the E element resulted in an approximately 50% reduction in X promoter activity in HuH7, HepG2, and HepSK cells. Deletional analysis showed that sequences upstream of the EF-C site (mp 1163) were required for full X promoter activity and implicated the NF-1a site as being sufficient for basal X promoter activity. However, PCR-directed linker scanning mutation of the NF-1a site did not cause a reduction in X promoter activity, indicating that this site was not an essential component of the X promoter. Taken together, these results indicated that multiple, partially redundant protein:DNA interactions in the enhancer I are essential for full X promoter activity. The lack of an essential basal promoter element supports the suggestion that the two separate HBV enhancer elements (enhI and enhII) were created by integration of the X gene into a primordial enhancer element.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chloramphenicol O-Acetyltransferase,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0042-6822
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
193
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
653-60
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:8384750-Base Sequence,
pubmed-meshheading:8384750-Carcinoma, Hepatocellular,
pubmed-meshheading:8384750-Cell Line,
pubmed-meshheading:8384750-Chloramphenicol O-Acetyltransferase,
pubmed-meshheading:8384750-DNA, Viral,
pubmed-meshheading:8384750-DNA-Binding Proteins,
pubmed-meshheading:8384750-Enhancer Elements, Genetic,
pubmed-meshheading:8384750-Genes, Viral,
pubmed-meshheading:8384750-Hepatitis B virus,
pubmed-meshheading:8384750-Humans,
pubmed-meshheading:8384750-Liver,
pubmed-meshheading:8384750-Liver Neoplasms,
pubmed-meshheading:8384750-Luciferases,
pubmed-meshheading:8384750-Molecular Sequence Data,
pubmed-meshheading:8384750-Mutagenesis, Insertional,
pubmed-meshheading:8384750-Oligodeoxyribonucleotides,
pubmed-meshheading:8384750-Plasmids,
pubmed-meshheading:8384750-Promoter Regions, Genetic,
pubmed-meshheading:8384750-Recombinant Proteins,
pubmed-meshheading:8384750-Restriction Mapping,
pubmed-meshheading:8384750-Sequence Deletion,
pubmed-meshheading:8384750-Tumor Cells, Cultured
|
pubmed:year |
1993
|
pubmed:articleTitle |
Characterization of the role of individual protein binding motifs within the hepatitis B virus enhancer I on X promoter activity using linker scanning mutagenesis.
|
pubmed:affiliation |
Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|