Linked Life Data

667935

Source:http://linkedlifedata.com/resource/pubmed/id/667935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1978-9-25
pubmed:abstractText
P3, a cell line derived from the plasmacytoma MOPC-21 secretes IgG1 (K) and is sensitive to complement (C')-mediated lysis by antibody directed against gamma1 or K. Sensitivity is attributed to the presence of immunoglobulin molecules on the surface membrane, designed Ig-mem. This sensitivity is abolished by antigenic modulation of Ig-mem. Modulated cells, when incubated in the absence of antibody, recover sensitivity to lysis in 4 hr. By measuring the rate of recovery, it has been possible to study the effects of various drugs on the reexpression of Ig-mem. Treatment of modulated cells with cycloheximide (Cx), pactamycin Pc), anisomycin (An), homoharringtonine (Ha) or sparsomycin (Sm), each a specific inhibitor of a different step in protein synthesis, produces a significant reduction in the rate of recovery. Paradoxically, puromycin (Pm), also a specific inhibitor of protein synthesis, does not reduce the rate of recovery. Studies were performed using Pm together with each of the other drugs to gain an understanding of the relationship between protein synthesis and recovery from modulation. Based upon these studies, we conclude that continued operation of the initiation cycle of protein synthesis is required for reexpression of Ig-mem in the absence of de novo protein formation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
33-42
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1978
pubmed:articleTitle
The effect of inhibitors of protein synthesis on the reexpression of surface immunoglobulin following antigenic modulation.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.