Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1991-1-16
pubmed:abstractText
Stimulation of T lymphocytes through their antigen receptor leads to the appearance of several transcription factors, including NF-AT and NF-kappa B, which are involved in regulating genes required for immunologic activation. To investigate the activity of a single transcription factor in individual viable cells, we have applied an assay that uses the fluorescence-activated cell sorter to quantitate beta-galactosidase (beta-gal). We have analyzed the distribution of NF-AT transcriptional activity among T cells undergoing activation by using a construct in which three tandem copies of the NF-AT-binding site directs transcription of the lacZ gene. Unexpectedly, stimulation of cloned stably transfected Jurkat T cells leads to a bimodal pattern of beta-gal expression in which some cells express no beta-gal and others express high levels. This expression pattern cannot be accounted for by cell-cycle position or heritable variation. Further results, in which beta-gal activity is correlated with NF-AT-binding activity, indicate that the concentration of NF-AT must exceed a critical threshold before transcription initiates. This threshold likely reflects the NF-AT concentration-dependent assembly of transcription complexes at the promoter. Similar constructs controlled by NF-kappa B or the entire interleukin-2 enhancer show bimodal expression patterns during induction, suggesting that thresholds set by the concentration of transcription factors may be a common property of inducible genes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0890-9369
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:geneSymbol
lacZ
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1823-34
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2123468-Cell Cycle, pubmed-meshheading:2123468-Cells, Cultured, pubmed-meshheading:2123468-Cinnamates, pubmed-meshheading:2123468-DNA-Binding Proteins, pubmed-meshheading:2123468-Drug Resistance, pubmed-meshheading:2123468-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:2123468-Gene Expression Regulation, pubmed-meshheading:2123468-Humans, pubmed-meshheading:2123468-Hygromycin B, pubmed-meshheading:2123468-Plasmids, pubmed-meshheading:2123468-Receptors, Antigen, T-Cell, pubmed-meshheading:2123468-Ribonucleases, pubmed-meshheading:2123468-Signal Transduction, pubmed-meshheading:2123468-T-Lymphocytes, pubmed-meshheading:2123468-Transcription, Genetic, pubmed-meshheading:2123468-Transcription Factors, pubmed-meshheading:2123468-Transfection, pubmed-meshheading:2123468-beta-Galactosidase
pubmed:year
1990
pubmed:articleTitle
Single cell assay of a transcription factor reveals a threshold in transcription activated by signals emanating from the T-cell antigen receptor.
pubmed:affiliation
Department of Genetics, Stanford University, California 94305.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.