Linked Life Data

2467945

Source:http://linkedlifedata.com/resource/pubmed/id/2467945

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1989-5-22
pubmed:abstractText
It has previously been reported that MHC class I-deficient RBL-5 and YAC-1 lymphoma sublines show an enhanced NK sensitivity in vitro. In the present study such lymphoma variants were found to have different defects in H-2 biosynthesis such as 1) reduced beta 2-microglobulin and H-2 H chain transcription, 2) block in beta 2-microglobulin translation, and 3) impaired association between beta 2-microglobulin and H-2 H chains. For lines with the latter two defects, the results suggested that a major part of the H chains were arrested before the middle Golgi complex as indicated by their failure to undergo carbohydrate side chain trimming. The data suggest that NK sensitivity can be directly influenced by the membrane expression of MHC class I gene products of tumor targets because three independent molecular defects, all interfering with the cell surface H-2 expression, gave rise to NK-sensitive phenotypes. These variant lines will also be useful tools for studies of H-2 glycoprotein assembly and transport and for Ag presentation to CTL.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2911-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Molecular analysis of H-2-deficient lymphoma lines. Distinct defects in biosynthesis and association of MHC class I heavy chains and beta 2-microglobulin observed in cells with increased sensitivity to NK cell lysis.
pubmed:affiliation
Department of Tumor Biology, Karolinska Institutet, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't