Linked Life Data

9067630

Source:http://linkedlifedata.com/resource/pubmed/id/9067630

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-6-24
pubmed:abstractText
Previous studies implicating a role for protein kinase C (PKC) in mediating stimulation of cellular responses by physiological agonists have relied on use of non-specific inhibitors or direct stimulation of PKC by phorbol esters. However, much of this evidence is questionable. Here, we have investigated the effects of a potent and selective PKC inhibitor, Ro 31-8425, on three different responses of human neutrophils stimulated by either a physiological agonist, C5a, or a phorbol ester, PMA. The responses studied were superoxide generation, collagenase secretion and adhesion to endothelial cells. In each case, the PMA-stimulated response was more sensitive to inhibition than the C5a-stimulated response. Even the PMA-stimulated responses differed in their sensitivity to inhibition, with superoxide production being the most sensitive and adhesion at least sensitive. The different sensitivities of the PMA stimulated responses suggest that, although activation of PKC stimulates the responses, either different degrees of activation or different isozymes are required for the different responses. The lower sensitivity of the C5a-stimulated responses in each case suggests that PKC activation, if needed at all, is not rate limiting in these signal transduction pathways. These results emphasize the redundancy in intracellular signal transduction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-7
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Different sensitivities of neutrophil responses to a selective protein kinase C inhibitor Ro 31-8425; redundancy in signal transduction.
pubmed:affiliation
Roche Research Centre, Welwyn Garden City, Herts, UK.
pubmed:publicationType
Journal Article