Linked Life Data

10438937

Source:http://linkedlifedata.com/resource/pubmed/id/10438937

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-9-9
pubmed:abstractText
IL-18 is expressed from a variety of cell types. Two promoters located upstream of exon 1 (5'-flanking region) and upstream of exon 2 (intron 1) regulate its expression. Both promoter regions were cloned into pCAT-Basic plasmid to yield p1-2686 for the 5'-flanking promoter and p2-2.3 for the intron 1 promoter. Both promoters showed basal constitutive activity and LPS inducibility when transfected into RAW 264.7 macrophages. To learn the regulatory elements of both promoters, 5'-serial deletion and site-directed mutants were prepared. For the activity of the p1-2686 promoter, the IFN consensus sequence binding protein (ICSBP) binding site between -39 and -22 was critical. EMSA using an oligonucleotide probe encompassing the ICSBP binding site showed that LPS treatment increased the formation of DNA binding complex. In addition, when supershift assays were performed, retardation of the protein-DNA complex was seen after the addition of anti-ICSBP Ab. For the activity of the p2-2.3 promoter, the PU.1 binding site between -31 and -13 was important. EMSA using a PU.1-specific oligonucleotide demonstrated that LPS treatment increased PU.1 binding activity. The addition of PU.1-specific Ab to LPS-treated nuclear extracts resulted in the formation of a supershifted complex. Furthermore, cotransfection of ICSBP or PU.1 expression vector increased p1 promoter activity or IL-18 expression, respectively. Taken together, these results indicate that ICSBP and PU.1 are critical elements for IL-18 gene expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2000-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10438937-5' Untranslated Regions, pubmed-meshheading:10438937-Animals, pubmed-meshheading:10438937-Binding Sites, pubmed-meshheading:10438937-Cell Line, pubmed-meshheading:10438937-Consensus Sequence, pubmed-meshheading:10438937-DNA, pubmed-meshheading:10438937-Gene Expression Regulation, pubmed-meshheading:10438937-Interferon Regulatory Factors, pubmed-meshheading:10438937-Interferons, pubmed-meshheading:10438937-Interleukin-18, pubmed-meshheading:10438937-Lipopolysaccharides, pubmed-meshheading:10438937-Mice, pubmed-meshheading:10438937-Mutagenesis, Site-Directed, pubmed-meshheading:10438937-Promoter Regions, Genetic, pubmed-meshheading:10438937-Proto-Oncogene Proteins, pubmed-meshheading:10438937-Repressor Proteins, pubmed-meshheading:10438937-Sequence Deletion, pubmed-meshheading:10438937-Trans-Activators, pubmed-meshheading:10438937-Transfection
pubmed:year
1999
pubmed:articleTitle
Roles of IFN consensus sequence binding protein and PU.1 in regulating IL-18 gene expression.
pubmed:affiliation
Immune Cell Signal Transduction RU, Korea Research Institute of Bioscience and Biotechnology, Taejon, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't