Linked Life Data

8304411

Source:http://linkedlifedata.com/resource/pubmed/id/8304411

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
1994-3-10
pubmed:abstractText
The expression of cytocidal activity is initiated by the interaction of macrophages with priming [e.g., interferon (IFN)] and triggering stimuli (polyinosinic-polycytidylic acid). We have shown that the triggering step can be initiated in a Ca(2+)-dependent fashion and hypothesized that protein kinase C (PKC) may couple the Ca2+ signal to the expression of a gene product, Bf, that accompanies the expression of macrophage cytocidal activity. Exposure of IFN-primed macrophages to polyinosinic-polycytidylic acid in the presence of the PKC inhibitors H-7 or sphingosine or after downregulation of PKC with phorbol myristate acetate markedly inhibited Bf synthesis. Western blots of macrophage lysates revealed the presence of the alpha-, delta-, and zeta-isozymes of PKC, and all were found to be downregulated by phorbol myristate acetate. Inhibition of PKC also prevented the increase in IFN-beta mRNA levels and partially blocked the response to IFN-beta. These data suggest that the alpha-, delta-, and zeta-isozymes of PKC are involved in signaling leading to Bf expression and that the level of involvement is restricted to the induction and response to IFN-beta.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C134-42
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Involvement of protein kinase C in macrophage activation by poly(I.C).
pubmed:affiliation
Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't