Linked Life Data

9574539

Source:http://linkedlifedata.com/resource/pubmed/id/9574539

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1998-5-21
pubmed:abstractText
The 5'-sequences flanking the human complement component C4 genes (C4A and C4B) have been analyzed for their ability to direct expression of a reporter gene in cell lines that constitutively express or do not express C4. No difference in the level of reporter gene expression was detected in cells transfected with C4A- or C4B-specific constructs. A series of reporter constructs containing progressively truncated C4 promoter fragments transfected into the hepatocyte Hep G2 cell line, identified the sequence contained within the region -178 to -39 as that associated with maximal reporter gene expression. This region contains consensus binding motifs for nuclear factor 1 (-110 to -97), Sp1 (-57 to -49), and three basic helix-loop-helix (-137 to -132, -98 to -93, and -78 to -73)-like transcription factors. Electromobility shift assays and DNase I footprinting analysis showed specific DNA-protein interactions of the C4 promoter at the nuclear factor 1, two E box (-98 to -93 and -78 to -73), and Sp1 binding domains. Site-directed mutagenesis of the Sp1 binding site resulted in total abrogation of reporter gene expression and mutation of the E box (-78 to -73) resulted in a 8-fold reduction in expression. We conclude that the Sp1 binding site at position -57 to -49 is critical for accurately initiated, basal transcription of C4.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4353-60
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Regulation of transcription of the TATA-less human complement component C4 gene.
pubmed:affiliation
Division of Medicine, Imperial College School of Medicine, London, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't