Statements in which the resource exists as a subject.
PredicateObject
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
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