Linked Life Data

7836405

Source:http://linkedlifedata.com/resource/pubmed/id/7836405

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-2-24
pubmed:databankReference
pubmed:abstractText
We have isolated and characterized regions important for expression of the mouse Na+/H+ exchanger gene. A 1.1-kilobase fragment upstream of the 5'-untranslated region contains specific DNA motifs characteristic of promoter and enhancer elements including a TATA box, two CAAT boxes, an SP-1 site, a cyclic AMP response element-binding site, and an AP-2-like site. This 1.1-kilobase fragment directs transcription of a luciferase reporter gene in mouse fibroblasts (NIH 3T3) and human Hep G2 cells. Deletion or mutation of an AP-2-like site 100 base pairs from the start site of transcription resulted in loss of most of the reporter plasmid activity. In addition, cotransfection of an AP-2 expression plasmid and the mouse promoter/luciferase plasmid increased the amount of Na+/H+ exchanger-directed transcription in AP-2-deficient Hep G2 cells. Moreover, mobility shift analysis indicated that a putative AP-2-binding site is capable of binding purified AP-2 protein and a specific protein from nuclear extracts of NIH 3T3 cells. The results show that the transcription factor AP-2 may play an important role in regulation of transcription of the mouse Na+/H+ exchanger gene.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
270
pubmed:geneSymbol
NHE-1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1375-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Activation of the Na+/H+ exchanger gene by the transcription factor AP-2.
pubmed:affiliation
Department of Pediatrics, Faculty of Medicine, University of Alberta, Edmonton, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't