Linked Life Data

8039828

Source:http://linkedlifedata.com/resource/pubmed/id/8039828

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-8-25
pubmed:abstractText
The kappa immunoglobulin (Igk) light chain locus is transcriptionally silent in the mouse B-cell lymphoma 70Z/3. However, exposure to lipopolysaccharide (LPS) or interferon-gamma (IFN) causes a marked increase in Igk transcription. By immunoselection, we isolated two variants that are nonresponsive to IFN. One variant, AT7.2, has retained its response to LPS (IFN-LPS+), whereas the other, AT3.3, is also nonresponsive to LPS (IFN-LPS-). Stable transfection of an intact Igk gene does not rescue the phenotype of either variant. Both variants have intact Igk genes and neither is deficient in the binding or uptake of IFN. Nuclear extracts from LPS-treated wild-type 70Z/3 cells show strong increases in three transcription factors: OTF-2, NF-kappa B, and kBF-A. Remarkably, when the IFN-LPS- variant is treated with LPS, all three transcription factors are still observed in the nuclear extracts. Treatment of wild-type cells with either LPS or IFN also causes a decrease in nuclear complexes that bind to two other regions of the Igk intron enhancer, the octenh and the E kappa MHCIC regions. Both of these changes are also observed after LPS or IFN treatment of the IFN-LPS- variant. Thus, this variant transduces the IFN and LPS signals at least into the nuclear compartment, but still fails to activate Igk transcription. In contrast, the IFN-LPS+ variant decreases neither the octenh nor the E kappa MHCIC binding complexes in response to IFN. This variant may be defective in transducing the IFN signal to the nucleus. These variants will be useful in studying the activation of Igk transcription and the IFN signaling pathway in B cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0093-7711
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
199-209
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8039828-Animals, pubmed-meshheading:8039828-B-Lymphocytes, pubmed-meshheading:8039828-Base Sequence, pubmed-meshheading:8039828-DNA, pubmed-meshheading:8039828-DNA-Binding Proteins, pubmed-meshheading:8039828-Down-Regulation, pubmed-meshheading:8039828-Enhancer Elements, Genetic, pubmed-meshheading:8039828-Genetic Variation, pubmed-meshheading:8039828-Immunoglobulin kappa-Chains, pubmed-meshheading:8039828-Interferon-gamma, pubmed-meshheading:8039828-Introns, pubmed-meshheading:8039828-Lipopolysaccharides, pubmed-meshheading:8039828-Mice, pubmed-meshheading:8039828-Molecular Sequence Data, pubmed-meshheading:8039828-NF-kappa B, pubmed-meshheading:8039828-Octamer Transcription Factor-2, pubmed-meshheading:8039828-Protein Binding, pubmed-meshheading:8039828-Signal Transduction, pubmed-meshheading:8039828-Tetradecanoylphorbol Acetate, pubmed-meshheading:8039828-Transcription, Genetic, pubmed-meshheading:8039828-Transcription Factors, pubmed-meshheading:8039828-Tumor Cells, Cultured
pubmed:year
1994
pubmed:articleTitle
Two different IFN-gamma nonresponsive variants derived from the B-cell lymphoma 70Z/3.
pubmed:affiliation
Department of Biological Structure, University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.