Linked Life Data

9202004

Source:http://linkedlifedata.com/resource/pubmed/id/9202004

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
27
pubmed:dateCreated
1997-7-31
pubmed:abstractText
The hepatitis B viral X promoter is known to be positively autoregulated by its own HBx protein, which also interacts with many cellular regulatory proteins. We investigated the effect of activating transcription factor 2 (ATF2) on the activity of the X promoter. Cotransfection of the ATF2 expression vector with a X promoter-chloramphenicol acetyltransferase plasmid repressed the X promoter activity in HepG2 cells. HBx activated activating protein 1 (AP-1)-mediated transcription through the hepatitis B virus E element by 35-fold, while its activation activity was inhibited in the presence of ATF2, suggesting that ATF2 inhibited the autoactivation of X promoter by HBx and basal transcription mediated by AP-1. Since the binding sites of AP-1 and ATF2 in the hepatitis B virus E element overlap, the repression of X promoter activity by ATF2 is exerted by the competition for the AP-1 binding site and the formation of the ATF2-Jun heterodimer as in the case of the consensus AP-1 element. However, the small X promoter had a ATF2 binding site and was activated by ATF2. These results suggest that the syntheses of X proteins are differentially regulated by ATF2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
4
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
16934-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Activating transcription factor 2 (ATF2) down-regulates hepatitis B virus X promoter activity by the competition for the activating protein 1 binding site and the formation of the ATF2-Jun heterodimer.
pubmed:affiliation
Department of Molecular Biology and Research Center for Cell Differentiation, Seoul National University, Seoul 151-742, Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't