Linked Life Data

7681061

Source:http://linkedlifedata.com/resource/pubmed/id/7681061

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1993-4-22
pubmed:abstractText
The mRNAs coding for interleukin-1 alpha (IL-1 alpha) and IL-1 beta are constitutively transcribed but do not accumulate in human diploid fibroblasts and in fibrosarcoma cells. Treatment of these cells with tumor necrosis factor (TNF) induces accumulation of IL-1 mRNA by an unknown mechanism. This induction of IL-1 mRNA was investigated in HT-1080 cells. The induction was quite fast, with maximum levels of IL-1 alpha and beta mRNA reached 4 h after addition of TNF. Nuclear run-off experiment showed that TNF did not increase the rate of transcription of IL-1 mRNA. This mRNA was apparently unstable in untreated cells, but it accumulated in cycloheximide-treated cells. Phorbol esters induced IL-1 mRNA, suggesting that activation of protein kinase C was responsible for the accumulation of this mRNA. This hypothesis was confirmed by experiments with the PKC inhibitors staurosporine and calphostin C, which prevented the induction of IL-1 mRNA by TNF and accelerated the decay of this mRNA in cells pretreated with TNF. Both IL-1 alpha and IL-1 beta were detected in TNF-treated cells by Western blot analysis and enzyme-linked immunosorbent assay. These results indicate that the TNF-mediated induction of IL-1 can be entirely accounted for by stabilization of this mRNA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6214-20
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Tumor necrosis factor increases stability of interleukin-1 mRNA by activating protein kinase C.
pubmed:affiliation
Department of Biological Sciences, State University of New York, Albany 12222.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.