Statements in which the resource exists as a subject.
PredicateObject
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
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