Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
|
pubmed:dateCreated |
1995-11-6
|
pubmed:databankReference | |
pubmed:abstractText |
Expression of the IgG Fc receptor type I (Fc gamma RI) on myeloid cells is dramatically increased by treatment with interferon-gamma (IFN-gamma). We observed that Fc gamma RI transcript levels in monoblast-like U937 cells were elevated within 3 hr and peaked 12 hr after exposure to IFN-gamma. Treatment of U937 with IFN-gamma for 9 hr in the presence of cycloheximide led to super-induction of Fc gamma RI expression. Nuclear run-on analysis revealed that the rate of Fc gamma RI transcription was increased by IFN-gamma. Genomic sequence upstream of the Fc gamma RIC gene was cloned and subjected to primer extension analysis, which demonstrated a single transcription initiation site without a TATA box. Transient transfections of CAT reporter gene constructs containing various Fc gamma RIC promoter sequences into U937 cells revealed that a 20-bp region surrounding the transcription start site (-7 to +13) was capable of mediating transcription initiation and that an IFN-gamma responsive element (GIRE) was present within 74 bp upstream of the transcription initiation site. A 17-bp sequence between positions -51 and -35 conferred IFN-gamma responsiveness on a heterologous promoter. Double-stranded GIRE sequence, but not a scrambled sequence, was specifically bound by nuclear proteins from IFN-gamma treated U937 cells. Gel shift experiments further showed that the STAT1 alpha protein bound to the Fc gamma RIC GIRE in response to IFN-gamma treatment of U937 cells. The Fc gamma RIC GIRE is homologous to the IFN-gamma activation sequence (GAS) of the guanylate binding protein and to X box elements of class II MHC genes. Our results demonstrate that transcriptional regulation of the Fc gamma RIC gene by IFN-gamma involves the binding of STAT1 alpha to a 17-bp GAS homology in the proximal promoter.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgG,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Stat1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0161-5890
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
32
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
841-51
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:7565811-Animals,
pubmed-meshheading:7565811-Base Sequence,
pubmed-meshheading:7565811-Binding Sites,
pubmed-meshheading:7565811-Cell Line,
pubmed-meshheading:7565811-DNA,
pubmed-meshheading:7565811-DNA Primers,
pubmed-meshheading:7565811-DNA-Binding Proteins,
pubmed-meshheading:7565811-Gene Expression Regulation,
pubmed-meshheading:7565811-Genes, MHC Class II,
pubmed-meshheading:7565811-Humans,
pubmed-meshheading:7565811-Interferon-gamma,
pubmed-meshheading:7565811-Mice,
pubmed-meshheading:7565811-Molecular Sequence Data,
pubmed-meshheading:7565811-Monocytes,
pubmed-meshheading:7565811-Promoter Regions, Genetic,
pubmed-meshheading:7565811-Receptors, IgG,
pubmed-meshheading:7565811-STAT1 Transcription Factor,
pubmed-meshheading:7565811-Sequence Homology, Nucleic Acid,
pubmed-meshheading:7565811-Trans-Activators,
pubmed-meshheading:7565811-Transcriptional Activation
|
pubmed:year |
1995
|
pubmed:articleTitle |
An interferon-gamma activation sequence mediates the transcriptional regulation of the IgG Fc receptor type IC gene by interferon-gamma.
|
pubmed:affiliation |
Division of Hematology/Oncology, UCLA School of Medicine, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|