Linked Life Data

1689272

Source:http://linkedlifedata.com/resource/pubmed/id/1689272

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-3-29
pubmed:abstractText
The mouse B-cell cell lymphoma 70Z/3 is a convenient model system in which to study the regulation of immunoglobulin synthesis. Three transcriptional activators of kappa (kappa) light chain synthesis have been identified for these cells: bacterial lipopolysaccharide (LPS), interferon-gamma (IFN), and interleukin-1 (IL-1). The response of the kappa gene in 70Z/3 cells to LPS is mediated by increases in two transcription factors: NF-kappa B and OTF-2. In contrast, IFN has no effect on either of these factors in 70Z/3 cells. We have isolated by immunoselection an LPS- IFN+ variant of 70Z/3 called 1.3E2. We show here that LPS treatment of these cells causes no increase in nuclear localization of either NF-kappa B or OTF-2. Although they have normal levels of cytoplasmic NF-kappa B, it cannot be activated by LPS or by phorbol 12-myristate 13-acetate (PMA) treatment of the cells. These experiments expand the genetic dissection of the molecular pathways of activation of kappa transcription in 70Z/3 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
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
1.3E2, a variant of the B lymphoma 70Z/3, defective in activation of NF-kappa B and OTF-2.
pubmed:affiliation
Department of Genetics (SK-50), University of Washington, Seattle 98195.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.