NDLI: Formation of stable transcription complexes as assayed by analysis of individual templates.

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Mechanism of inhibitory effect of dextran sulfate and heparin on replication of human immunodeficiency virus in vitro.

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Activation of protein kinase C differentially modulates neuronal Na+, Ca2+, and gamma-aminobutyrate type A channels.

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Characterization of the gene for the a subunit of human factor XIII (plasma transglutaminase), a blood coagulation factor.

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Molecular characterization of T-cell antigen receptor expression by subsets of CD4- CD8- murine thymocytes.

Reexpression of a developmentally regulated antigen in Down syndrome and Alzheimer disease.

Formation of stable transcription complexes as assayed by analysis of individual templates.

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Phosphorylation of Alzheimer disease amyloid precursor peptide by protein kinase C and Ca2+/calmodulin-dependent protein kinase II.

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Statistical geometry in sequence space: a method of quantitative comparative sequence analysis.

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Genetic analysis of indefinite division in human cells: identification of four complementation groups.

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Sequence and organization of the diversity, joining, and constant region genes of the human T-cell delta-chain locus.

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Formation of stable transcription complexes as assayed by analysis of individual templates.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Weintraub, H.
Description	Author Affiliation: Weintraub H ( Fred Hutchinson Cancer Research Center, Seattle, WA 98104.);
Abstract	Conditions were established where transient transfection of two marker genes resulted in the expression of one or the other, but not both, in individual cells as assayed by immunofluorescence. Thus, the expression from a single cell reflects the activity of single active transcription templates. Under these conditions, a vector encoding the simian virus 40 large tumor antigen (SV40 T-Ag) driven by the SV40 enhancer and early promoter was transfected into CV-1, L, or HeLa cells yielding, for all three cell types, about 10-30% T-Ag-positive cells as assayed by immunofluorescence. Similar vectors containing either mutated or deleted SV40 enhancers also gave T-Ag-positive cells, but at about 1/100 the frequency. Quantitative analysis showed that T-Ag-positive cells produced about the same amount of T-Ag whether or not an active enhancer was present. Chloramphenicol acetyltransferase-encoding vectors gave the same result. The data are consistent with the hypothesis that at a low, but finite, probability, fully functional transcription complexes can form on a given active template in the absence of enhancer DNA. Enhancers seem to increase the number of active templates. Subcloning experiments suggest that these transcription complexes can be surprisingly stable.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	16
Volume Number	85
Language	English
Publisher	National Academy of Sciences
Publisher Date	1988-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Templates, Genetic Transcription, Genetic Acetyltransferases Genetics Antigens, Viral, Tumor Chloramphenicol O-Acetyltransferase Enhancer Elements, Genetic Fluorescent Antibody Technique Recombination, Genetic Transfection Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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