Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-6-14
pubmed:databankReference
pubmed:abstractText
Arginine metabolism in macrophages during infection and inflammation is complex, owing to differential regulation of inducible nitric oxide synthase (iNOS) and arginases by cytokines and other agents. Changes in levels of Th2 cytokines such as interleukin-4 (IL-4) can play important roles in these conditions via effects on arginine metabolism. IL-4 alters macrophage arginine metabolism by inducing arginase I expression and inhibiting nitric oxide production. To determine the molecular basis for induction of arginase I, the promoter of the murine arginase I gene was cloned and analyzed by transfection in RAW 264.7 macrophage cells. IL-4 induction required a composite response element containing STAT6 and C/EBP sites located 2.86 kb upstream of the transcription start site. Competition experiments showed that STAT6 and C/EBPbeta bind to the STAT6 and C/EBP sites non-cooperatively. Elucidation of the mechanisms involved in regulation of arginase I transcription may provide a basis for developing strategies to modulate arginase expression in Th2 cytokine-predominant diseases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0378-1119
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
353
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
98-106
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15922518-Animals, pubmed-meshheading:15922518-Arginase, pubmed-meshheading:15922518-Base Sequence, pubmed-meshheading:15922518-Binding, Competitive, pubmed-meshheading:15922518-Binding Sites, pubmed-meshheading:15922518-CCAAT-Enhancer-Binding Protein-beta, pubmed-meshheading:15922518-Cell Line, pubmed-meshheading:15922518-DNA, pubmed-meshheading:15922518-Electrophoretic Mobility Shift Assay, pubmed-meshheading:15922518-Gene Expression Regulation, Enzymologic, pubmed-meshheading:15922518-Interleukin-4, pubmed-meshheading:15922518-Luciferases, pubmed-meshheading:15922518-Macrophages, pubmed-meshheading:15922518-Mice, pubmed-meshheading:15922518-Mice, Inbred Strains, pubmed-meshheading:15922518-Molecular Sequence Data, pubmed-meshheading:15922518-Promoter Regions, Genetic, pubmed-meshheading:15922518-Protein Binding, pubmed-meshheading:15922518-Recombinant Fusion Proteins, pubmed-meshheading:15922518-Response Elements, pubmed-meshheading:15922518-STAT6 Transcription Factor, pubmed-meshheading:15922518-Sequence Homology, Nucleic Acid, pubmed-meshheading:15922518-Trans-Activators, pubmed-meshheading:15922518-Transcription, Genetic, pubmed-meshheading:15922518-Transfection
pubmed:year
2005
pubmed:articleTitle
Induction of arginase I transcription by IL-4 requires a composite DNA response element for STAT6 and C/EBPbeta.
pubmed:affiliation
Department of Molecular Genetics and Biochemistry, W1255 Biomedical Science Tower, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural